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Book Details
Abstract
The 13th edition of Guyton and Hall Textbook of Medical Physiology continues this bestselling title's long tradition as the world’s foremost medical physiology textbook. Unlike other textbooks on this topic, this clear and comprehensive guide has a consistent, single-author voice and focuses on the content most relevant to clinical and pre-clinical students. The detailed but lucid text is complemented by didactic illustrations that summarize key concepts in physiology and pathophysiology.
- Emphasizes core information around how the body must maintain homeostasis in order to remain healthy, while supporting information and examples are detailed.
- Summary figures and tables help quickly convey key processes covered in the text.
- Reflects the latest advances in molecular biology and cardiovascular, neurophysiology and gastrointestinal topics.
- Bold full-color drawings and diagrams.
- Short, easy-to-read, masterfully edited chapters and a user-friendly full-color design.
- Clinical vignettes throughout the text all you to see core concepts applied to real-life situations.
- Brand-new quick-reference chart of normal lab values included.
- Increased number of figures, clinical correlations, and cellular and molecular mechanisms important for clinical medicine.
- Medicine eBook is accessible on a variety of devices.
Table of Contents
| Section Title | Page | Action | Price |
|---|---|---|---|
| Front Cover | cover | ||
| IFC_Student Consult ad | IFC1 | ||
| IE_IFC_Student Consult ad | IFC2 | ||
| Guyton and Hall Textbook of Medical Physiology | i | ||
| Copyright Page | iv | ||
| Dedication | v | ||
| Preface | vii | ||
| Table Of Contents | ix | ||
| Half title page | xxi | ||
| Unit I Introduction to Physiology: The Cell and General Physiology | 1 | ||
| 1 Functional Organization of the Human Body and Control of the “Internal Environment” | 3 | ||
| Human Physiology. | 3 | ||
| Cells are the Living Units of the Body | 3 | ||
| Extracellular Fluid—the “Internal Environment” | 3 | ||
| Differences Between Extracellular and Intracellular Fluids. | 3 | ||
| Homeostasis—Maintenance of A Nearly Constant Internal Environment | 4 | ||
| Extracellular Fluid Transport and Mixing System—the Blood Circulatory System | 4 | ||
| Origin of Nutrients in the Extracellular Fluid | 5 | ||
| Respiratory System. | 5 | ||
| Gastrointestinal Tract. | 5 | ||
| Liver and Other Organs That Perform Primarily Metabolic Functions. | 5 | ||
| Musculoskeletal System. | 5 | ||
| Removal of Metabolic End Products | 5 | ||
| Removal of Carbon Dioxide by the Lungs. | 5 | ||
| Kidneys. | 5 | ||
| Gastrointestinal Tract. | 6 | ||
| Liver. | 6 | ||
| Regulation of Body Functions | 6 | ||
| Nervous System. | 6 | ||
| Hormone Systems. | 6 | ||
| Protection of the Body | 6 | ||
| Immune System. | 6 | ||
| Integumentary System. | 6 | ||
| Reproduction | 6 | ||
| Control Systems of the Body | 6 | ||
| Examples of Control Mechanisms | 7 | ||
| Regulation of Oxygen and Carbon Dioxide Concentrations in the Extracellular Fluid. | 7 | ||
| Regulation of Arterial Blood Pressure. | 7 | ||
| Normal Ranges and Physical Characteristics of Important Extracellular Fluid Constituents | 7 | ||
| Characteristics of Control Systems | 8 | ||
| Negative Feedback Nature of Most Control Systems | 8 | ||
| Gain of a Control System. | 8 | ||
| Positive Feedback Can Sometimes Cause Vicious Cycles and Death | 9 | ||
| Positive Feedback Can Sometimes Be Useful. | 9 | ||
| More Complex Types of Control Systems—Adaptive Control | 9 | ||
| Summary—Automaticity of the Body | 10 | ||
| Bibliography | 10 | ||
| 2 The Cell and Its Functions | 11 | ||
| Organization of the Cell | 11 | ||
| Water. | 11 | ||
| Ions. | 11 | ||
| Proteins. | 11 | ||
| Lipids. | 11 | ||
| Carbohydrates. | 12 | ||
| Physical Structure of the Cell | 12 | ||
| Membranous Structures of the Cell | 12 | ||
| Cell Membrane | 12 | ||
| The Cell Membrane Lipid Barrier Impedes Penetration by Water-Soluble Substances. | 12 | ||
| Integral and Peripheral Cell Membrane Proteins. | 13 | ||
| Membrane Carbohydrates—The Cell “Glycocalyx.” | 14 | ||
| Cytoplasm and its Organelles | 14 | ||
| Endoplasmic Reticulum | 14 | ||
| Ribosomes and the Granular Endoplasmic Reticulum. | 15 | ||
| Agranular Endoplasmic Reticulum. | 15 | ||
| Golgi Apparatus | 15 | ||
| Lysosomes | 15 | ||
| Peroxisomes | 16 | ||
| Secretory Vesicles | 16 | ||
| Mitochondria | 16 | ||
| Cell Cytoskeleton—Filament and Tubular Structures | 17 | ||
| Nucleus | 17 | ||
| Nuclear Membrane. | 17 | ||
| Nucleoli and Formation of Ribosomes. | 18 | ||
| Comparison of the Animal Cell with Precellular Forms of Life | 18 | ||
| Functional Systems of the Cell | 19 | ||
| Ingestion by the Cell—Endocytosis | 19 | ||
| Pinocytosis. | 19 | ||
| Phagocytosis. | 19 | ||
| Pinocytotic and Phagocytic Foreign Substances are Digested Inside the Cell by Lysosomes | 20 | ||
| Regression of Tissues and Autolysis of Damaged Cells. | 20 | ||
| Recycling of Cell Organelles—Autophagy. | 20 | ||
| Synthesis of Cellular Structures by Endoplasmic Reticulum and Golgi Apparatus | 20 | ||
| Specific Functions of the Endoplasmic Reticulum | 20 | ||
| Proteins Are Formed by the Granular Endoplasmic Reticulum. | 21 | ||
| Synthesis of Lipids by the Smooth Endoplasmic Reticulum. | 21 | ||
| Other Functions of the Endoplasmic Reticulum. | 21 | ||
| Specific Functions of the Golgi Apparatus | 21 | ||
| Synthetic Functions of the Golgi Apparatus. | 21 | ||
| Processing of Endoplasmic Secretions by the Golgi Apparatus—Formation of Vesicles. | 21 | ||
| Types of Vesicles Formed by the Golgi Apparatus—Secretory Vesicles and Lysosomes. | 22 | ||
| Use of Intracellular Vesicles to Replenish Cellular Membranes. | 22 | ||
| The Mitochondria Extract Energy from Nutrients | 22 | ||
| Functional Characteristics of ATP | 23 | ||
| Chemical Processes in the Formation of ATP—Role of the Mitochondria. | 23 | ||
| Uses of ATP for Cellular Function. | 23 | ||
| Locomotion of Cells | 24 | ||
| Ameboid Movement | 24 | ||
| Mechanism of Ameboid Locomotion. | 24 | ||
| Types of Cells That Exhibit Ameboid Locomotion. | 25 | ||
| Control of Ameboid Locomotion—Chemotaxis. | 25 | ||
| Cilia and Ciliary Movements | 25 | ||
| Mechanism of Ciliary Movement. | 26 | ||
| Bibliography | 26 | ||
| 3 Genetic Control of Protein Synthesis, Cell Function, and Cell Reproduction | 27 | ||
| Genes in the Cell Nucleus Control Protein Synthesis | 27 | ||
| Basic Building Blocks of DNA | 27 | ||
| Nucleotides | 27 | ||
| Nucleotides Are Organized to Form Two Strands of DNA Loosely Bound to Each Other | 28 | ||
| Genetic Code | 29 | ||
| The DNA Code in the Cell Nucleus is Transferred to RNA Code in the Cell Cytoplasm—The Process of Transcription | 30 | ||
| Rna is Synthesized in the Nucleus from a DNA Template | 30 | ||
| Basic Building Blocks of RNA. | 30 | ||
| Formation of RNA Nucleotides. | 30 | ||
| “Activation” of the RNA Nucleotides. | 30 | ||
| Assembly of the RNA Chain from Activated Nucleotides Using the DNA Strand as a Template—The Process of Transcription | 30 | ||
| There Are Several Different Types of RNA. | 31 | ||
| Messenger RNA—The Codons | 31 | ||
| RNA Codons for the Different Amino Acids. | 31 | ||
| Transfer RNA—The Anticodons | 32 | ||
| Ribosomal RNA | 32 | ||
| Formation of Ribosomes in the Nucleolus. | 32 | ||
| miRNA and Small Interfering RNA | 32 | ||
| Formation of Proteins on the Ribosomes—The Process of Translation | 33 | ||
| Polyribosomes. | 33 | ||
| Many Ribosomes Attach to the Endoplasmic Reticulum. | 34 | ||
| Chemical Steps in Protein Synthesis. | 34 | ||
| Peptide Linkage. | 35 | ||
| Synthesis of Other Substances in the Cell | 35 | ||
| Control of Gene Function and Biochemical Activity in Cells | 35 | ||
| Genetic Regulation | 35 | ||
| The Promoter Controls Gene Expression. | 35 | ||
| Other Mechanisms for Control of Transcription by the Promoter. | 36 | ||
| Control of Intracellular Function by Enzyme Regulation | 37 | ||
| Enzyme Inhibition. | 37 | ||
| Enzyme Activation. | 37 | ||
| Summary. | 37 | ||
| The DNA–Genetic System Controls Cell Reproduction | 37 | ||
| Life Cycle of the Cell | 37 | ||
| Cell Reproduction Begins With Replication of DNA | 37 | ||
| Chemical and Physical Events of DNA Replication. | 38 | ||
| DNA Repair, DNA “Proofreading,” and “Mutation.” | 38 | ||
| Chromosomes and Their Replication | 38 | ||
| Cell Mitosis | 39 | ||
| Mitotic Apparatus: Function of the Centrioles. | 39 | ||
| Prophase. | 39 | ||
| Prometaphase. | 39 | ||
| Metaphase. | 39 | ||
| Anaphase. | 39 | ||
| Telophase. | 39 | ||
| Control of Cell Growth and Cell Reproduction | 40 | ||
| Telomeres Prevent the Degradation of Chromosomes. | 40 | ||
| Regulation of Cell Size. | 41 | ||
| Cell Differentiation | 41 | ||
| Apoptosis—Programmed Cell Death | 41 | ||
| Cancer | 41 | ||
| Invasive Characteristic of the Cancer Cell. | 42 | ||
| Why Do Cancer Cells Kill? | 43 | ||
| Bibliography | 43 | ||
| Unit II Membrane Physiology, Nerve, and Muscle | 45 | ||
| 4 Transport of Substances Through Cell Membranes | 47 | ||
| The Cell Membrane Consists of a Lipid Bilayer with Cell Membrane Transport Proteins | 47 | ||
| “Diffusion” Versus “Active Transport.” | 47 | ||
| Diffusion | 47 | ||
| Diffusion Through the Cell Membrane | 48 | ||
| Diffusion of Lipid-Soluble Substances Through the Lipid Bilayer. | 48 | ||
| Diffusion of Water and Other Lipid-Insoluble Molecules Through Protein Channels. | 48 | ||
| Diffusion Through Protein Pores and Channels—Selective Permeability and “Gating” of Channels | 49 | ||
| Selective Permeability of Protein Channels. | 49 | ||
| Gating of Protein Channels. | 50 | ||
| Open-State Versus Closed-State of Gated Channels. | 50 | ||
| Patch-Clamp Method for Recording Ion Current Flow Through Single Channels. | 50 | ||
| Facilitated Diffusion Requires Membrane Carrier Proteins | 51 | ||
| Factors that Affect Net Rate of Diffusion | 52 | ||
| Net Diffusion Rate Is Proportional to the Concentration Difference Across a Membrane. | 52 | ||
| Effect of Membrane Electrical Potential on Diffusion of Ions—The “Nernst Potential.” | 52 | ||
| Effect of a Pressure Difference Across the Membrane. | 53 | ||
| Osmosis Across Selectively Permeable Membranes—“Net Diffusion” of Water | 53 | ||
| Osmotic Pressure | 53 | ||
| Importance of Number of Osmotic Particles (Molar Concentration) in Determining Osmotic Pressure. | 54 | ||
| “Osmolality”—The Osmole. | 54 | ||
| Relation of Osmolality to Osmotic Pressure. | 54 | ||
| The Term “Osmolarity.” | 54 | ||
| “Active Transport” of Substances Through Membranes | 54 | ||
| Primary Active Transport and Secondary Active Transport. | 55 | ||
| Primary Active Transport | 55 | ||
| Sodium-Potassium Pump Transports Sodium Ions Out of Cells and Potassium Ions Into Cells | 55 | ||
| The Na+-K+ Pump Is Important for Controlling Cell Volume. | 56 | ||
| Electrogenic Nature of the Na+-K+ Pump. | 56 | ||
| Primary Active Transport of Calcium Ions | 56 | ||
| Primary Active Transport of Hydrogen Ions | 56 | ||
| Energetics of Primary Active Transport | 56 | ||
| Secondary Active Transport—Co-Transport and Counter-Transport | 57 | ||
| Co-Transport of Glucose and Amino Acids Along with Sodium Ions | 57 | ||
| Sodium Counter-Transport of Calcium and Hydrogen Ions | 57 | ||
| Active Transport Through Cellular Sheets | 58 | ||
| Bibliography | 58 | ||
| 5 Membrane Potentials and Action Potentials | 61 | ||
| Basic Physics of Membrane Potentials | 61 | ||
| Membrane Potentials Caused by Ion Concentration | 61 | ||
| Differences Across a Selectively Permeable Membrane | 61 | ||
| The Nernst Equation Describes the Relation of Diffusion Potential to the Ion Concentration Difference Across a Membrane. | 61 | ||
| The Goldman Equation Is Used to Calculate the Diffusion Potential When the Membrane Is Permeable to Several Different Ions. | 62 | ||
| Measuring the Membrane Potential | 62 | ||
| Resting Membrane Potential of Neurons | 63 | ||
| Active Transport of Sodium and Potassium Ions Through the Membrane—The Sodium-Potassium (Na+-K+) Pump. | 63 | ||
| Leakage of Potassium Through the Nerve Cell Membrane. | 63 | ||
| Origin of the Normal Resting Membrane Potential | 64 | ||
| Contribution of the Potassium Diffusion Potential. | 64 | ||
| Contribution of Sodium Diffusion Through the Nerve Membrane. | 64 | ||
| Contribution of the Na+-K+ Pump. | 64 | ||
| Neuron Action Potential | 65 | ||
| Resting Stage. | 65 | ||
| Depolarization Stage. | 65 | ||
| Repolarization Stage. | 65 | ||
| Voltage-Gated Sodium and Potassium Channels | 65 | ||
| Activation and Inactivation of the Voltage-Gated Sodium Channel | 65 | ||
| Activation of the Sodium Channel. | 65 | ||
| Inactivation of the Sodium Channel. | 66 | ||
| Voltage-Gated Potassium Channel and Its Activation | 66 | ||
| The “Voltage Clamp” Method for Measuring the Effect of Voltage on Opening and Closing of the Voltage-Gated Channels. | 66 | ||
| Summary of the Events that Cause the Action Potential | 67 | ||
| Roles of Other Ions During the Action Potential | 68 | ||
| Impermeant Negatively Charged Ions (Anions) Inside the Nerve Axon. | 68 | ||
| Calcium Ions. | 68 | ||
| Increased Permeability of the Sodium Channels When There Is a Deficit of Calcium Ions. | 68 | ||
| Initiation of the Action Potential | 68 | ||
| A Positive-Feedback Cycle Opens the Sodium Channels. | 68 | ||
| Threshold for Initiation of the Action Potential. | 69 | ||
| Propagation of the Action Potential | 69 | ||
| Direction of Propagation. | 69 | ||
| All-or-Nothing Principle. | 69 | ||
| Re-Establishing Sodium and Potassium Ionic Gradients After Action Potentials are Completed—Importance of Energy Metabolism | 69 | ||
| Plateau in Some Action Potentials | 70 | ||
| Rhythmicity of Some Excitable Tissues—Repetitive Discharge | 70 | ||
| Re-excitation Process Necessary for Spontaneous Rhythmicity. | 71 | ||
| Special Characteristics of Signal Transmission in Nerve Trunks | 71 | ||
| Myelinated and Unmyelinated Nerve Fibers. | 71 | ||
| “Saltatory” Conduction in Myelinated Fibers from Node to Node. | 72 | ||
| Velocity of Conduction in Nerve Fibers. | 72 | ||
| Excitation—The Process of Eliciting the Action Potential | 72 | ||
| Excitation of a Nerve Fiber by a Negatively Charged Metal Electrode. | 73 | ||
| Threshold for Excitation and “Acute Local Potentials.” | 73 | ||
| “Refractory Period” After an Action Potential, During Which a New Stimulus Cannot be Elicited | 73 | ||
| Inhibition of Excitability—“Stabilizers” and Local Anesthetics | 73 | ||
| Local Anesthetics. | 73 | ||
| Bibliography | 74 | ||
| 6 Contraction of Skeletal Muscle | 75 | ||
| Physiological Anatomy of Skeletal Muscle | 75 | ||
| Skeletal Muscle Fiber | 75 | ||
| The Sarcolemma Is a Thin Membrane Enclosing a Skeletal Muscle Fiber. | 75 | ||
| Myofibrils Are Composed of Actin and Myosin Filaments. | 75 | ||
| Titin Filamentous Molecules Keep the Myosin and Actin Filaments in Place. | 75 | ||
| Sarcoplasm Is the Intracellular Fluid between Myofibrils. | 77 | ||
| Sarcoplasmic Reticulum Is a Specialized Endoplasmic Reticulum of Skeletal Muscle. | 77 | ||
| General Mechanism of Muscle Contraction | 77 | ||
| Molecular Mechanism of Muscle Contraction | 78 | ||
| Muscle Contraction Occurs by a Sliding Filament Mechanism. | 78 | ||
| Molecular Characteristics of the Contractile Filaments | 78 | ||
| Myosin Filaments Are Composed of Multiple Myosin Molecules. | 78 | ||
| Adenosine Triphosphatase Activity of the Myosin Head. | 79 | ||
| Actin Filaments Are Composed of Actin, Tropomyosin, and Troponin. | 79 | ||
| Tropomyosin Molecules. | 79 | ||
| Troponin and Its Role in Muscle Contraction. | 79 | ||
| Interaction of One Myosin Filament, Two Actin Filaments, and Calcium Ions to Cause Contraction | 79 | ||
| Inhibition of the Actin Filament by the Troponin-Tropomyosin Complex. | 79 | ||
| Activation of the Actin Filament by Calcium Ions. | 80 | ||
| Interaction of the “Activated” Actin Filament and the Myosin Cross-Bridges—The “Walk-Along” Theory of Contraction. | 80 | ||
| ATP as the Energy Source for Contraction—Chemical Events in the Motion of the Myosin Heads. | 80 | ||
| The Amount of Actin and Myosin Filament Overlap Determines Tension Developed by the Contracting Muscle | 81 | ||
| Effect of Muscle Length on Force of Contraction in the Whole Intact Muscle. | 81 | ||
| Relation of Velocity of Contraction to Load | 81 | ||
| Energetics of Muscle Contraction | 82 | ||
| Work Output during Muscle Contraction | 82 | ||
| Three Sources of Energy for Muscle Contraction | 82 | ||
| Efficiency of Muscle Contraction. | 83 | ||
| Characteristics of Whole Muscle Contraction | 83 | ||
| Isometric Contractions Do Not Shorten Muscle, Whereas Isotonic Contractions Shorten Muscle at a Constant Tension. | 83 | ||
| Characteristics of Isometric Twitches Recorded from Different Muscles. | 83 | ||
| Fast Versus Slow Muscle Fibers. | 84 | ||
| Slow Fibers (Type 1, Red Muscle). | 84 | ||
| Fast Fibers (Type II, White Muscle). | 84 | ||
| Mechanics of Skeletal Muscle Contraction | 84 | ||
| Motor Unit—All the Muscle Fibers Innervated by a Single Nerve Fiber. | 84 | ||
| Muscle Contractions of Different Force—Force Summation. | 84 | ||
| Multiple Fiber Summation. | 85 | ||
| Frequency Summation and Tetanization. | 85 | ||
| Maximum Strength of Contraction. | 85 | ||
| Changes in Muscle Strength at the Onset of Contraction—The Staircase Effect (Treppe). | 85 | ||
| Skeletal Muscle Tone. | 86 | ||
| Muscle Fatigue. | 86 | ||
| Lever Systems of the Body. | 86 | ||
| “Positioning” of a Body Part by Contraction of Agonist and Antagonist Muscles on Opposite Sides of a Joint—“Coactivation” of Antagonist Muscles. | 86 | ||
| Remodeling of Muscle to Match Function | 87 | ||
| Muscle Hypertrophy and Muscle Atrophy. | 87 | ||
| Adjustment of Muscle Length. | 87 | ||
| Hyperplasia of Muscle Fibers. | 87 | ||
| Muscle Denervation Causes Rapid Atrophy. | 87 | ||
| Recovery of Muscle Contraction in Poliomyelitis: Development of Macromotor Units. | 87 | ||
| Rigor Mortis. | 88 | ||
| Muscular Dystrophy. | 88 | ||
| Bibliography | 88 | ||
| 7 Excitation of Skeletal Muscle: | 89 | ||
| Transmission of Impulses from Nerve Endings to Skeletal Muscle Fibers: the Neuromuscular Junction | 89 | ||
| Physiologic Anatomy of the Neuromuscular Junction—the Motor End Plate | 89 | ||
| Secretion of Acetylcholine by the Nerve Terminals | 89 | ||
| Acetylcholine Opens Ion Channels on Postsynaptic Membranes. | 89 | ||
| Destruction of the Released Acetylcholine by Acetylcholinesterase. | 91 | ||
| End Plate Potential and Excitation of the Skeletal Muscle Fiber. | 91 | ||
| Safety Factor for Transmission at the Neuromuscular Junction; Fatigue of the Junction. | 92 | ||
| Molecular Biology of Acetylcholine Formation and Release | 92 | ||
| Drugs That Enhance or Block Transmission at the Neuromuscular Junction | 92 | ||
| Drugs That Stimulate the Muscle Fiber by Acetylcholine-Like Action. | 92 | ||
| Drugs That Stimulate the Neuromuscular Junction by Inactivating Acetylcholinesterase. | 92 | ||
| Drugs That Block Transmission at the Neuromuscular Junction. | 93 | ||
| Myasthenia Gravis Causes Muscle Weakness | 93 | ||
| Muscle Action Potential | 93 | ||
| Action Potentials Spread to the Interior of the Muscle Fiber by Way of “Transverse Tubules” | 93 | ||
| Excitation-Contraction Coupling | 93 | ||
| Transverse Tubule–Sarcoplasmic Reticulum System | 93 | ||
| Release of Calcium Ions by the Sarcoplasmic Reticulum | 93 | ||
| A Calcium Pump Removes Calcium Ions from the Myofibrillar Fluid After Contraction Occurs. | 94 | ||
| Excitatory “Pulse” of Calcium Ions. | 94 | ||
| Bibliography | 95 | ||
| 8 Excitation and Contraction of Smooth Muscle | 97 | ||
| Contraction of Smooth Muscle | 97 | ||
| Types of Smooth Muscle | 97 | ||
| Multi-Unit Smooth Muscle. | 97 | ||
| Unitary Smooth Muscle. | 97 | ||
| Contractile Mechanism in Smooth Muscle | 97 | ||
| Chemical Basis for Smooth Muscle Contraction | 97 | ||
| Physical Basis for Smooth Muscle Contraction | 98 | ||
| Comparison of Smooth Muscle Contraction and Skeletal Muscle Contraction | 98 | ||
| Slow Cycling of the Myosin Cross-Bridges. | 99 | ||
| Low Energy Requirement to Sustain Smooth Muscle Contraction. | 99 | ||
| Slowness of Onset of Contraction and Relaxation of the Total Smooth Muscle Tissue. | 99 | ||
| The Maximum Force of Contraction Is Often Greater in Smooth Muscle Than in Skeletal Muscle. | 99 | ||
| The “Latch” Mechanism Facilitates Prolonged Holding of Contractions of Smooth Muscle. | 99 | ||
| Stress-Relaxation of Smooth Muscle. | 99 | ||
| Regulation of Contraction by Calcium Ions | 99 | ||
| Calcium Ions Combine with Calmodulin to Cause Activation of Myosin Kinase and Phosphorylation of the Myosin Head. | 100 | ||
| Source of Calcium Ions That Cause Contraction | 100 | ||
| Role of the Smooth Muscle Sarcoplasmic Reticulum. | 100 | ||
| Smooth Muscle Contraction Is Dependent on Extracellular Calcium Ion Concentration. | 101 | ||
| A Calcium Pump Is Required to Cause Smooth Muscle Relaxation. | 101 | ||
| Myosin Phosphatase Is Important in Cessation of Contraction. | 101 | ||
| Possible Mechanism for Regulation of the Latch Phenomenon. | 101 | ||
| Nervous and Hormonal Control of Smooth Muscle Contraction | 102 | ||
| Neuromuscular Junctions of Smooth Muscle | 102 | ||
| Physiologic Anatomy of Smooth Muscle Neuromuscular Junctions. | 102 | ||
| Excitatory and Inhibitory Transmitter Substances Secreted at the Smooth Muscle Neuromuscular Junction. | 102 | ||
| Membrane Potentials and Action Potentials in Smooth Muscle | 103 | ||
| Membrane Potentials in Smooth Muscle. | 103 | ||
| Action Potentials in Unitary Smooth Muscle. | 103 | ||
| Spike Potentials. | 103 | ||
| Action Potentials with Plateaus. | 103 | ||
| Calcium Channels Are Important in Generating the Smooth Muscle Action Potential. | 103 | ||
| Slow Wave Potentials in Unitary Smooth Muscle Can Lead to Spontaneous Generation of Action Potentials. | 103 | ||
| Excitation of Visceral Smooth Muscle by Muscle Stretch. | 104 | ||
| Depolarization of Multi-Unit Smooth Muscle Without Action Potentials | 104 | ||
| Effect of Local Tissue Factors and Hormones to Cause Smooth Muscle Contraction Without Action Potentials | 104 | ||
| Smooth Muscle Contraction in Response to Local Tissue Chemical Factors. | 104 | ||
| Effects of Hormones on Smooth Muscle Contraction. | 104 | ||
| Mechanisms of Smooth Muscle Excitation or Inhibition by Hormones or Local Tissue Factors. | 104 | ||
| Bibliography | 105 | ||
| Unit III The Heart | 107 | ||
| 9 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves | 109 | ||
| Physiology of Cardiac Muscle | 109 | ||
| Physiologic Anatomy of Cardiac Muscle | 109 | ||
| Cardiac Muscle Is a Syncytium. | 109 | ||
| Action Potentials in Cardiac Muscle | 110 | ||
| What Causes the Long Action Potential and the Plateau? | 110 | ||
| Summary of Phases of Cardiac Muscle Action Potential. | 111 | ||
| Velocity of Signal Conduction in Cardiac Muscle. | 111 | ||
| Refractory Period of Cardiac Muscle. | 111 | ||
| Excitation-Contraction Coupling—Function of Calcium Ions and the Transverse Tubules | 112 | ||
| Duration of Contraction. | 112 | ||
| Cardiac Cycle | 113 | ||
| Diastole and Systole | 113 | ||
| Increasing Heart Rate Decreases Duration of Cardiac Cycle. | 113 | ||
| Relationship of the Electrocardiogram to the Cardiac Cycle | 114 | ||
| The Atria Function as Primer Pumps for the Ventricles | 114 | ||
| Pressure Changes in the Atria—a, c, and v Waves. | 114 | ||
| Function of the Ventricles as Pumps | 115 | ||
| The Ventricles Fill With Blood During Diastole. | 115 | ||
| Outflow of Blood From the Ventricles During Systole | 115 | ||
| Period of Isovolumic (Isometric) Contraction. | 115 | ||
| Period of Ejection. | 115 | ||
| Period of Isovolumic (Isometric) Relaxation. | 115 | ||
| End-Diastolic Volume, End-Systolic Volume, and Stroke Volume Output. | 115 | ||
| The Heart Valves Prevent Backflow of Blood During Systole | 115 | ||
| Atrioventricular Valves. | 115 | ||
| Function of the Papillary Muscles. | 116 | ||
| Aortic and Pulmonary Artery Valves. | 116 | ||
| Aortic Pressure Curve | 116 | ||
| Relationship of the Heart Sounds to Heart Pumping | 116 | ||
| Work Output of the Heart | 116 | ||
| Graphical Analysis of Ventricular Pumping | 117 | ||
| “Volume-Pressure Diagram” During the Cardiac Cycle; Cardiac Work Output. | 117 | ||
| Concepts of Preload and Afterload. | 118 | ||
| Chemical Energy Required for Cardiac Contraction: Oxygen Utilization by the Heart | 118 | ||
| Efficiency of Cardiac Contraction. | 119 | ||
| Regulation of Heart Pumping | 119 | ||
| Intrinsic Regulation of Heart Pumping—The Frank-Starling Mechanism | 119 | ||
| What Is the Explanation of the Frank-Starling Mechanism? | 119 | ||
| Ventricular Function Curves | 119 | ||
| Control of the Heart by the Sympathetic and Parasympathetic Nerves | 120 | ||
| Mechanisms of Excitation of the Heart by the Sympathetic Nerves. | 120 | ||
| Parasympathetic (Vagal) Stimulation Reduces Heart Rate and Strength of Contraction. | 120 | ||
| Effect of Sympathetic or Parasympathetic Stimulation on the Cardiac Function Curve. | 120 | ||
| Effect of Potassium and Calcium Ions on Heart Function | 121 | ||
| Effect of Potassium Ions. | 121 | ||
| Effect of Calcium Ions. | 121 | ||
| Effect of Temperature on Heart Function | 121 | ||
| Increasing the Arterial Pressure Load (Up to a Limit) Does Not Decrease the Cardiac Output | 121 | ||
| Bibliography | 122 | ||
| 10 Rhythmical Excitation of the Heart | 123 | ||
| Specialized Excitatory and Conductive System of the Heart | 123 | ||
| Sinus (Sinoatrial) Node | 123 | ||
| Automatic Electrical Rhythmicity of the Sinus Fibers | 123 | ||
| Mechanism of Sinus Nodal Rhythmicity. | 123 | ||
| Self-Excitation of Sinus Nodal Fibers. | 124 | ||
| Internodal and Interatrial Pathways Transmit Cardiac Impulses Through the Atria | 125 | ||
| The Atrioventricular Node Delays Impulse Conduction from the Atria to the Ventricles | 125 | ||
| Cause of the Slow Conduction. | 125 | ||
| Rapid Transmission in the Ventricular Purkinje System | 125 | ||
| One-Way Conduction Through the A-V Bundle. | 126 | ||
| Distribution of the Purkinje Fibers in the Ventricles—The Left and Right Bundle Branches. | 126 | ||
| Transmission of the Cardiac Impulse in the Ventricular Muscle | 126 | ||
| Summary of the Spread of the Cardiac Impulse Through the Heart | 126 | ||
| Control of Excitation and Conduction in the Heart | 126 | ||
| The Sinus Node is the Normal Pacemaker of the Heart | 126 | ||
| Abnormal Pacemakers—“Ectopic” Pacemaker. | 127 | ||
| Role of the Purkinje System in Causing Synchronous Contraction of the Ventricular Muscle | 127 | ||
| Sympathetic and Parasympathetic Nerves Control Heart Rhythmicity and Impulse Conduction by the Cardiac Nerves | 128 | ||
| Parasympathetic (Vagal) Stimulation Slows the Cardiac Rhythm and Conduction. | 128 | ||
| Mechanism of the Vagal Effects. | 128 | ||
| Sympathetic Stimulation Increases the Cardiac Rhythm and Conduction. | 128 | ||
| Mechanism of the Sympathetic Effect. | 128 | ||
| Bibliography | 129 | ||
| 11 The Normal Electrocardiogram | 131 | ||
| Characteristics of the Normal Electrocardiogram | 131 | ||
| Depolarization Waves Versus Repolarization Waves | 131 | ||
| Relation of the Monophasic Action Potential of Ventricular Muscle to the QRS and T Waves in the Standard Electrocardiogram. | 131 | ||
| Relationship of Atrial and Ventricular Contraction to the Waves of the Electrocardiogram | 132 | ||
| Voltage and Time Calibration of the Electrocardiogram | 133 | ||
| Normal Voltages in the Electrocardiogram. | 133 | ||
| P-Q or P-R Interval. | 133 | ||
| Q-T Interval. | 133 | ||
| Rate of Heartbeat as Determined from the Electrocardiogram. | 133 | ||
| Flow of Current Around the Heart During the Cardiac Cycle | 133 | ||
| Recording Electrical Potentials from a Partially Depolarized Mass of Syncytial Cardiac Muscle | 133 | ||
| Flow of Electrical Currents in the Chest Around the Heart | 134 | ||
| Electrocardiographic Leads | 134 | ||
| Three Bipolar Limb Leads | 134 | ||
| Lead I. | 134 | ||
| Lead II. | 135 | ||
| Lead III. | 135 | ||
| Einthoven’s Triangle. | 135 | ||
| Einthoven’s Law. | 135 | ||
| Normal Electrocardiograms Recorded from the Three Standard Bipolar Limb Leads. | 135 | ||
| Chest Leads (Precordial Leads) | 136 | ||
| Augmented Unipolar Limb Leads | 136 | ||
| Methods for Recording Electrocardiograms | 137 | ||
| Ambulatory Electrocardiography | 137 | ||
| Bibliography | 137 | ||
| 12 Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities: | 139 | ||
| Principles of Vectorial Analysis of Electrocardiograms | 139 | ||
| Use of Vectors to Represent Electrical Potentials | 139 | ||
| “Resultant” Vector in the Heart at Any Given Instant. | 139 | ||
| The Direction of a Vector is Denoted in Terms of Degrees | 139 | ||
| Axis for Each Standard Bipolar Lead and Each Unipolar Limb Lead | 140 | ||
| Vectorial Analysis of Potentials Recorded in Different Leads | 140 | ||
| Vectorial Analysis of Potentials in the Three Standard Bipolar Limb Leads. | 141 | ||
| Vectorial Analysis of the Normal Electrocardiogram | 141 | ||
| Vectors that Occur at Successive Intervals During Depolarization of the Ventricles—The QRS Complex | 141 | ||
| Electrocardiogram During Repolarization—The T Wave | 143 | ||
| Depolarization of the Atria—The P Wave | 143 | ||
| Repolarization of the Atria—the Atrial T Wave. | 144 | ||
| Vectorcardiogram | 144 | ||
| Mean Electrical Axis of the Ventricular QRS and Its Significance | 144 | ||
| Determining the Electrical Axis from Standard Lead Electrocardiograms | 144 | ||
| Abnormal Ventricular Conditions that Cause Axis Deviation | 145 | ||
| Change in the Position of the Heart in the Chest. | 145 | ||
| Hypertrophy of One Ventricle. | 145 | ||
| Vectorial Analysis of Left Axis Deviation Resulting from Hypertrophy of the Left Ventricle. | 145 | ||
| Vectorial Analysis of Right Axis Deviation Resulting from Hypertrophy of the Right Ventricle. | 146 | ||
| Bundle Branch Block Causes Axis Deviation. | 146 | ||
| Vectorial Analysis of Left Axis Deviation in Left Bundle Branch Block. | 146 | ||
| Vectorial Analysis of Right Axis Deviation in Right Bundle Branch Block. | 146 | ||
| Conditions that Cause Abnormal Voltages of the QRS Complex | 147 | ||
| Increased Voltage in the Standard Bipolar Limb Leads | 147 | ||
| Decreased Voltage of the Electrocardiogram | 147 | ||
| Decreased Voltage Caused by Cardiac Myopathies. | 147 | ||
| Decreased Voltage Caused by Conditions Surrounding the Heart. | 147 | ||
| Prolonged and Bizarre Patterns of the QRS Complex | 148 | ||
| Cardiac Hypertrophy or Dilation Prolong the QRS Complex | 148 | ||
| Purkinje System Block Prolongs the QRS Complex | 148 | ||
| Conditions that Cause Bizarre QRS Complexes | 148 | ||
| Current of Injury | 148 | ||
| Effect of Current of Injury on the QRS Complex | 148 | ||
| The “J Point” is the Zero Reference Potential for Analyzing Current of Injury | 149 | ||
| Use of the J Point in Plotting Axis of Injury Potential. | 150 | ||
| Coronary Ischemia as a Cause of Injury Potential | 150 | ||
| Acute Anterior Wall Infarction. | 150 | ||
| Posterior Wall Infarction. | 151 | ||
| Infarction in Other Parts of the Heart. | 151 | ||
| Recovery from Acute Coronary Thrombosis. | 151 | ||
| Old Recovered Myocardial Infarction. | 152 | ||
| Current of Injury in Angina Pectoris. | 152 | ||
| Abnormalities in the T Wave | 152 | ||
| Effect of Slow Conduction of the Depolarization Wave on the Characteristics of the T Wave | 152 | ||
| Shortened Depolarization in Portions of the Ventricular Muscle Can Cause T-Wave Abnormalities | 152 | ||
| Effect of Digitalis on the T Wave. | 153 | ||
| Bibliography | 153 | ||
| 13 Cardiac Arrhythmias and Their Electrocardiographic Interpretation | 155 | ||
| Abnormal Sinus Rhythms | 155 | ||
| Tachycardia | 155 | ||
| Bradycardia | 155 | ||
| Bradycardia in Athletes. | 155 | ||
| Vagal Stimulation Causes Bradycardia. | 155 | ||
| Sinus Arrhythmia | 156 | ||
| Abnormal Rhythms that Result from Block of Heart Signals within the Intracardiac Conduction Pathways | 156 | ||
| Sinoatrial Block | 156 | ||
| Atrioventricular Block | 156 | ||
| Incomplete Atrioventricular Heart Block | 156 | ||
| Prolonged P-R (or P-Q) Interval—First-Degree Block. | 156 | ||
| Second-Degree Block. | 157 | ||
| Complete A-V Block (Third-Degree Block). | 157 | ||
| Stokes-Adams Syndrome—Ventricular Escape. | 157 | ||
| Incomplete Intraventricular Block—Electrical Alternans | 158 | ||
| Premature Contractions | 158 | ||
| Causes Of Premature Contractions | 158 | ||
| Premature Atrial Contractions | 158 | ||
| Pulse Deficit. | 158 | ||
| A-V Nodal or A-V Bundle Premature Contractions | 158 | ||
| Premature Ventricular Contractions | 159 | ||
| Vector Analysis of the Origin of an Ectopic Premature Ventricular Contraction. | 159 | ||
| Disorders of Cardiac Repolarization—The Long QT Syndromes. | 159 | ||
| Paroxysmal Tachycardia | 160 | ||
| Atrial Paroxysmal Tachycardia | 160 | ||
| A-V Nodal Paroxysmal Tachycardia. | 161 | ||
| Ventricular Paroxysmal Tachycardia | 161 | ||
| Ventricular Fibrillation | 161 | ||
| Phenomenon of Re-Entry—“Circus Movements” as the Basis for Ventricular Fibrillation | 161 | ||
| Chain Reaction Mechanism of Fibrillation | 162 | ||
| Fibrillation Caused by 60-Cycle Alternating Current. | 162 | ||
| Electrocardiogram in Ventricular Fibrillation | 163 | ||
| Electroshock Defibrillation of the Ventricles | 163 | ||
| Hand Pumping of the Heart (Cardiopulmonary Resuscitation) as an Aid to Defibrillation | 164 | ||
| Atrial Fibrillation | 164 | ||
| Impaired Pumping of the Atria During Atrial Fibrillation. | 164 | ||
| Electrocardiogram in Atrial Fibrillation | 164 | ||
| Irregularity of Ventricular Rhythm During Atrial Fibrillation | 165 | ||
| Electroshock Treatment of Atrial Fibrillation | 165 | ||
| Atrial Flutter | 165 | ||
| Cardiac Arrest | 165 | ||
| Bibliography | 165 | ||
| Unit IV The Circulation | 167 | ||
| 14 Overview of the Circulation; Biophysics of Pressure, Flow, and Resistance | 169 | ||
| Physical Characteristics of the Circulation | 169 | ||
| Functional Parts of the Circulation. | 169 | ||
| Volumes of Blood in the Different Parts of the Circulation. | 169 | ||
| Cross-Sectional Areas and Velocities of Blood Flow. | 169 | ||
| Pressures in the Various Portions of the Circulation. | 170 | ||
| Basic Principles of Circulatory Function | 170 | ||
| Interrelationships of Pressure, Flow, and Resistance | 171 | ||
| Blood Flow | 172 | ||
| Methods for Measuring Blood Flow. | 172 | ||
| Electromagnetic Flowmeter. | 172 | ||
| Ultrasonic Doppler Flowmeter. | 173 | ||
| Laminar Flow of Blood in Vessels. | 173 | ||
| Parabolic Velocity Profile During Laminar Flow. | 173 | ||
| Turbulent Flow of Blood Under Some Conditions. | 173 | ||
| Blood Pressure | 174 | ||
| Standard Units of Pressure. | 174 | ||
| High-Fidelity Methods for Measuring Blood Pressure. | 174 | ||
| Resistance to Blood Flow | 175 | ||
| Units of Resistance. | 175 | ||
| Expression of Resistance in CGS Units. | 175 | ||
| Total Peripheral Vascular Resistance and Total Pulmonary Vascular Resistance. | 175 | ||
| “Conductance” of Blood in a Vessel Is the Reciprocal of Resistance. | 175 | ||
| Small Changes in Vessel Diameter Markedly Change Its Conductance. | 175 | ||
| Poiseuille’s Law. | 175 | ||
| Importance of the Vessel Diameter “Fourth Power Law” in Determining Arteriolar Resistance. | 176 | ||
| Resistance to Blood Flow in Series and Parallel Vascular Circuits. | 176 | ||
| Effect of Blood Hematocrit and Blood Viscosity on Vascular Resistance and Blood Flow | 177 | ||
| Hematocrit—the Proportion of Blood That Is Red Blood Cells. | 177 | ||
| Increasing Hematocrit Markedly Increases Blood Viscosity. | 177 | ||
| Effects of Pressure on Vascular Resistance and Tissue Blood Flow | 177 | ||
| “Autoregulation” Attenuates the Effect of Arterial Pressure on Tissue Blood Flow. | 177 | ||
| Pressure-Flow Relationship in Passive Vascular Beds. | 178 | ||
| Bibliography | 178 | ||
| 15 Vascular Distensibility and Functions of the Arterial and Venous Systems | 179 | ||
| Vascular Distensibility | 179 | ||
| Units of Vascular Distensibility. | 179 | ||
| The Veins Are Much More Distensible Than the Arteries. | 179 | ||
| Vascular Compliance (or Vascular Capacitance) | 179 | ||
| Volume-Pressure Curves of the Arterial and Venous Circulations | 179 | ||
| Effect of Sympathetic Stimulation or Sympathetic Inhibition on the Volume-Pressure Relations of the Arterial and Venous Systems. | 180 | ||
| Delayed Compliance (Stress-Relaxation) of Vessels | 180 | ||
| Arterial Pressure Pulsations | 180 | ||
| Abnormal Pressure Pulse Contours | 181 | ||
| Transmission of Pressure Pulses to the Peripheral Arteries | 181 | ||
| Pressure Pulses Are Damped in the Smaller Arteries, Arterioles, and Capillaries. | 181 | ||
| Clinical Methods for Measuring Systolic and Diastolic Pressures | 182 | ||
| Auscultatory Method. | 182 | ||
| Normal Arterial Pressures as Measured by the Auscultatory Method. | 183 | ||
| Mean Arterial Pressure. | 183 | ||
| Veins and Their Functions | 184 | ||
| Venous Pressures—Right Atrial Pressure (Central Venous Pressure) and Peripheral Venous Pressures | 184 | ||
| Venous Resistance and Peripheral Venous Pressure | 184 | ||
| Effect of High Right Atrial Pressure on Peripheral Venous Pressure. | 185 | ||
| Effect of Intra-abdominal Pressure on Venous Pressures of the Leg. | 185 | ||
| Effect of Gravitational Pressure on Venous Pressure | 185 | ||
| Effect of the Gravitational Factor on Arterial and Other Pressures. | 186 | ||
| Venous Valves and the “Venous Pump”: Their Effects on Venous Pressure | 186 | ||
| Venous Valve Incompetence Causes “Varicose” Veins. | 186 | ||
| Clinical Estimation of Venous Pressure. | 186 | ||
| Direct Measurement of Venous Pressure and Right Atrial Pressure. | 186 | ||
| Pressure Reference Level for Measuring Venous and Other Circulatory Pressures. | 187 | ||
| Blood Reservoir Function of the Veins | 187 | ||
| Specific Blood Reservoirs | 187 | ||
| The Spleen as a Reservoir for Storing Red Blood Cells | 187 | ||
| Blood-Cleansing Function of the Spleen—Removal of Old Cells | 188 | ||
| Reticuloendothelial Cells of the Spleen | 188 | ||
| Bibliography | 188 | ||
| 16 The Microcirculation and Lymphatic System: | 189 | ||
| Structure of the Microcirculation and Capillary System | 189 | ||
| Structure of the Capillary Wall. | 189 | ||
| “Pores” in the Capillary Membrane. | 189 | ||
| Special Types of “Pores” Occur in the Capillaries of Certain Organs. | 190 | ||
| Flow of Blood in the Capillaries—Vasomotion | 190 | ||
| Regulation of Vasomotion. | 190 | ||
| Average Function of the Capillary System. | 191 | ||
| Exchange of Water, Nutrients, and Other Substances between the Blood and Interstitial Fluid | 191 | ||
| Diffusion Through the Capillary Membrane | 191 | ||
| Lipid-Soluble Substances Diffuse Directly Through the Cell Membranes of the Capillary Endothelium. | 191 | ||
| Water-Soluble, Non–Lipid-Soluble Substances Diffuse Through Intercellular “Pores” in the Capillary Membrane. | 191 | ||
| Effect of Molecular Size on Passage Through the Pores. | 191 | ||
| Effect of Concentration Difference on Net Rate of Diffusion Through the Capillary Membrane. | 192 | ||
| Interstitium and Interstitial Fluid | 192 | ||
| “Gel” in the Interstitium. | 193 | ||
| “Free” Fluid in the Interstitium. | 193 | ||
| Fluid Filtration Across Capillaries is Determined by Hydrostatic and Colloid Osmotic Pressures and the Capillary Filtration Coefficient | 193 | ||
| Hydrostatic and Colloid Osmotic Forces Determine Fluid Movement Through the Capillary Membrane. | 193 | ||
| Capillary Hydrostatic Pressure | 194 | ||
| Micropipette Method for Measuring Capillary Pressure. | 194 | ||
| Isogravimetric Method for Indirectly Measuring “Functional” Capillary Pressure. | 194 | ||
| Interstitial Fluid Hydrostatic Pressure | 195 | ||
| Measurement of Interstitial Fluid Pressure Using the Micropipette. | 195 | ||
| Measurement of Interstitial Free Fluid Pressure in Implanted Perforated Hollow Capsules. | 195 | ||
| Interstitial Fluid Pressures in Tightly Encased Tissues. | 195 | ||
| Summary: Interstitial Fluid Pressure in Loose Subcutaneous Tissue Is Usually Subatmospheric. | 195 | ||
| Pumping by the Lymphatic System Is the Basic Cause of the Negative Interstitial Fluid Pressure. | 195 | ||
| Plasma Colloid Osmotic Pressure | 195 | ||
| Plasma Proteins Cause Colloid Osmotic Pressure. | 195 | ||
| Normal Values for Plasma Colloid Osmotic Pressure. | 196 | ||
| Effect of the Different Plasma Proteins on Colloid Osmotic Pressure. | 196 | ||
| Interstitial Fluid Colloid Osmotic Pressure | 196 | ||
| Exchange of Fluid Volume Through the Capillary Membrane | 196 | ||
| Analysis of the Forces Causing Filtration at the Arterial End of the Capillary. | 196 | ||
| Analysis of Reabsorption at the Venous End of the Capillary. | 196 | ||
| Starling Equilibrium for Capillary Exchange | 197 | ||
| Capillary Filtration Coefficient | 197 | ||
| Effect of Abnormal Imbalance of Forces at the Capillary Membrane. | 197 | ||
| Lymphatic System | 198 | ||
| Lymph Channels of the Body | 198 | ||
| Terminal Lymphatic Capillaries and Their Permeability. | 199 | ||
| Formation of Lymph | 199 | ||
| Rate of Lymph Flow | 199 | ||
| Effect of Interstitial Fluid Pressure on Lymph Flow. | 199 | ||
| Lymphatic Pump Increases Lymph Flow. | 200 | ||
| Pumping Caused by External Intermittent Compression of the Lymphatics. | 200 | ||
| Lymphatic Capillary Pump. | 200 | ||
| Summary of Factors That Determine Lymph Flow. | 201 | ||
| The Lymphatic System Plays a Key Role in Controlling Interstitial Fluid Protein Concentration, Volume, and Pressure | 201 | ||
| Significance of Negative Interstitial Fluid Pressure as a Means for Holding the Body Tissues Together | 201 | ||
| Bibliography | 201 | ||
| 17 Local and Humoral Control of Tissue Blood Flow | 203 | ||
| Local Control of Blood Flow in Response to Tissue Needs | 203 | ||
| Variations in Blood Flow in Different Tissues and Organs. | 203 | ||
| Importance of Blood Flow Control by the Local Tissues. | 203 | ||
| Mechanisms of Blood Flow Control | 203 | ||
| Acute Control of Local Blood Flow | 204 | ||
| Increases in Tissue Metabolism Increase Tissue Blood Flow | 204 | ||
| Reduced Oxygen Availability Increases Tissue Blood Flow. | 204 | ||
| Vasodilator Theory for Acute Local Blood Flow Regulation—Possible Special Role of Adenosine. | 204 | ||
| Oxygen Demand Theory for Local Blood Flow Control. | 205 | ||
| Possible Role of Other Nutrients Besides Oxygen in Control of Local Blood Flow. | 205 | ||
| Special Examples of Acute “Metabolic” Control of Local Blood Flow | 206 | ||
| “Reactive Hyperemia” Occurs after the Tissue Blood Supply Is Blocked for a Short Time. | 206 | ||
| “Active Hyperemia” Occurs When Tissue Metabolic Rate Increases. | 206 | ||
| Autoregulation of Blood Flow During Changes in Arterial Pressure—“Metabolic” and “Myogenic” Mechanisms | 206 | ||
| Special Mechanisms for Acute Blood Flow Control in Specific Tissues | 207 | ||
| Control of Tissue Blood Flow by Endothelial-Derived Relaxing or Constricting Factors | 208 | ||
| Nitric Oxide—A Vasodilator Released from Healthy Endothelial Cells. | 208 | ||
| Endothelin—A Powerful Vasoconstrictor Released from Damaged Endothelium. | 208 | ||
| Long-Term Blood Flow Regulation | 209 | ||
| Blood Flow Regulation by Changes in Tissue Vascularity | 209 | ||
| Role of Oxygen in Long-Term Regulation. | 210 | ||
| Importance of Vascular Growth Factors in Formation of New Blood Vessels. | 210 | ||
| Vascularity Is Determined by Maximum Blood Flow Need, Not by Average Need. | 210 | ||
| Blood Flow Regulation by Development of Collateral Circulation | 210 | ||
| Vascular Remodeling in Response to Chronic Changes in Blood Flow or Blood Pressure | 211 | ||
| Humoral Control of the Circulation | 212 | ||
| Vasoconstrictor Agents | 212 | ||
| Norepinephrine and Epinephrine. | 212 | ||
| Angiotensin II. | 212 | ||
| Vasopressin. | 212 | ||
| Vasodilator Agents | 213 | ||
| Bradykinin. | 213 | ||
| Histamine. | 213 | ||
| Vascular Control by Ions and Other Chemical Factors | 213 | ||
| Most Vasodilators or Vasoconstrictors Have Little Effect on Long-Term Blood Flow Unless They Alter the Metabolic Rate of the Tissues. | 213 | ||
| Bibliography | 213 | ||
| 18 Nervous Regulation of the Circulation and Rapid Control of Arterial Pressure | 215 | ||
| Nervous Regulation of the Circulation | 215 | ||
| Autonomic Nervous System | 215 | ||
| Sympathetic Nervous System. | 215 | ||
| Sympathetic Innervation of the Blood Vessels. | 215 | ||
| Sympathetic Stimulation Increases Heart Rate and Contractility. | 215 | ||
| Parasympathetic Stimulation Decreases Heart Rate and Contractility. | 215 | ||
| Sympathetic Vasoconstrictor System and Its Control by the Central Nervous System | 216 | ||
| Vasomotor Center in the Brain and Its Control of the Vasoconstrictor System. | 216 | ||
| Continuous Partial Constriction of the Blood Vessels Is Normally Caused by Sympathetic Vasoconstrictor Tone. | 217 | ||
| Control of Heart Activity by the Vasomotor Center. | 217 | ||
| Control of the Vasomotor Center by Higher Nervous Centers. | 217 | ||
| Norepinephrine Is the Sympathetic Vasoconstrictor Neurotransmitter. | 218 | ||
| Adrenal Medullae and Their Relation to the Sympathetic Vasoconstrictor System. | 218 | ||
| Sympathetic Vasodilator System and Its Control by the Central Nervous System. | 218 | ||
| Possible Role of the Sympathetic Vasodilator System. | 218 | ||
| Emotional Fainting—Vasovagal Syncope. | 218 | ||
| Role of the Nervous System in Rapid Control of Arterial Pressure | 218 | ||
| Nervous Control of Arterial Pressure Is Rapid. | 218 | ||
| Increases in Arterial Pressure during Muscle Exercise and Other Types of Stress | 219 | ||
| Reflex Mechanisms for Maintaining Normal Arterial Pressure | 219 | ||
| Baroreceptor Arterial Pressure Control System—Baroreceptor Reflexes | 219 | ||
| Physiologic Anatomy of the Baroreceptors and Their Innervation. | 219 | ||
| Response of the Baroreceptors to Arterial Pressure. | 219 | ||
| Circulatory Reflex Initiated by the Baroreceptors. | 219 | ||
| The Baroreceptors Attenuate Blood Pressure Changes During Changes in Body Posture. | 221 | ||
| Pressure “Buffer” Function of the Baroreceptor Control System. | 221 | ||
| Are the Baroreceptors Important in Long-Term Regulation of Arterial Pressure? | 222 | ||
| Control of Arterial Pressure by the Carotid and Aortic Chemoreceptors—Effect of Low Oxygen on Arterial Pressure. | 222 | ||
| Atrial and Pulmonary Artery Reflexes Regulate Arterial Pressure. | 222 | ||
| Atrial Reflexes That Activate the Kidneys—The “Volume Reflex.” | 222 | ||
| Atrial Reflex Control of Heart Rate (the Bainbridge Reflex). | 223 | ||
| CNS Ischemic Response—Control of Arterial Pressure by the Brain’S Vasomotor Center in Response to Diminished Brain Blood Flow | 223 | ||
| Importance of the CNS Ischemic Response as a Regulator of Arterial Pressure. | 223 | ||
| Cushing Reaction to Increased Pressure Around the Brain. | 223 | ||
| Special Features of Nervous Control of Arterial Pressure | 224 | ||
| Role of the Skeletal Nerves and Skeletal Muscles in Increasing Cardiac Output and Arterial Pressure | 224 | ||
| Abdominal Compression Reflex. | 224 | ||
| Increased Cardiac Output and Arterial Pressure Caused by Skeletal Muscle Contraction During Exercise. | 224 | ||
| Respiratory Waves in the Arterial Pressure | 224 | ||
| Arterial Pressure “Vasomotor” Waves—Oscillation of Pressure Reflex Control Systems | 224 | ||
| Oscillation of the Baroreceptor and Chemoreceptor Reflexes. | 224 | ||
| Oscillation of the CNS Ischemic Response. | 225 | ||
| Bibliography | 225 | ||
| 19 Role of the Kidneys in Long-Term Control of Arterial Pressure and in Hypertension: | 227 | ||
| Renal–Body Fluid System for Arterial Pressure Control | 227 | ||
| Quantitation of Pressure Diuresis as a Basis for Arterial Pressure Control | 227 | ||
| An Experiment Demonstrating the Renal–Body Fluid System for Arterial Pressure Control. | 227 | ||
| The Renal–Body Fluid Mechanism Provides Nearly Infinite Feedback Gain for Long-term Arterial Pressure Control. | 228 | ||
| Two Key Determinants of Long-Term Arterial Pressure. | 228 | ||
| The Chronic Renal Output Curve Is Much Steeper than the Acute Curve. | 229 | ||
| Failure of Increased Total Peripheral Resistance to Elevate the Long-Term Level of Arterial Pressure if Fluid Intake and Renal Function Do Not Change | 230 | ||
| Increased Fluid Volume Can Elevate Arterial Pressure by Increasing Cardiac Output or Total Peripheral Resistance | 230 | ||
| Importance of Salt (NaCl) in the Renal–Body Fluid Schema for Arterial Pressure Regulation | 231 | ||
| Chronic Hypertension (High Blood Pressure) is Caused by Impaired Renal Function | 232 | ||
| Experimental Volume-Loading Hypertension Caused by Reduced Renal Mass With Simultaneous Increase in Salt Intake. | 232 | ||
| Sequential Changes in Circulatory Function During the Development of Volume-Loading Hypertension. | 232 | ||
| Volume-Loading Hypertension in Patients Who Have No Kidneys but Are Being Maintained with an Artificial Kidney | 234 | ||
| Hypertension Caused by Excess Aldosterone | 234 | ||
| The Renin-Angiotensin System: Its Role in Arterial Pressure Control | 234 | ||
| Components of the Renin-Angiotensin System | 234 | ||
| Rapidity and Intensity of the Vasoconstrictor Pressure Response to the Renin-Angiotensin System | 235 | ||
| Angiotensin II Causes Renal Retention of Salt and Water—An Important Means for Long-Term Control of Arterial Pressure | 235 | ||
| Mechanisms of the Direct Renal Effects of Angiotensin II to Cause Renal Retention of Salt and Water. | 236 | ||
| Angiotensin II Increases Kidney Salt and Water Retention by Stimulating Aldosterone. | 236 | ||
| Quantitative Analysis of Arterial Pressure Changes Caused by Angiotensin II. | 236 | ||
| Role of the Renin-Angiotensin System in Maintaining a Normal Arterial Pressure Despite Large Variations in Salt Intake | 236 | ||
| Types of Hypertension in which Angiotensin is Involved: Hypertension Caused by a Renin-Secreting Tumor or by Renal Ischemia | 237 | ||
| “One-Kidney” Goldblatt Hypertension. | 237 | ||
| “Two-Kidney” Goldblatt Hypertension. | 238 | ||
| Hypertension Caused by Diseased Kidneys That Secrete Renin Chronically. | 238 | ||
| Other Types of Hypertension Caused by Combinations of Volume Loading and Vasoconstriction | 238 | ||
| Hypertension in the Upper Part of the Body Caused by Coarctation of the Aorta. | 238 | ||
| Role of Autoregulation in Hypertension Caused by Aortic Coarctation. | 239 | ||
| Hypertension in Preeclampsia (Toxemia of Pregnancy). | 239 | ||
| Neurogenic Hypertension. | 239 | ||
| Genetic Causes of Hypertension. | 239 | ||
| Primary (Essential) Hypertension | 240 | ||
| Graphical Analysis of Arterial Pressure Control in Essential Hypertension. | 240 | ||
| Treatment of Essential Hypertension. | 241 | ||
| Summary of the Integrated, Multifaceted System for Arterial Pressure Regulation | 241 | ||
| Rapidly Acting Pressure Control Mechanisms That Act Within Seconds or Minutes. | 241 | ||
| Pressure Control Mechanisms That Act After Many Minutes. | 242 | ||
| Long-Term Mechanisms for Arterial Pressure Regulation. | 242 | ||
| Bibliography | 243 | ||
| 20 Cardiac Output, Venous Return, and Their Regulation | 245 | ||
| Normal Values for Cardiac Output at Rest and During Activity | 245 | ||
| Cardiac Index | 245 | ||
| Effect of Age on Cardiac Output. | 245 | ||
| Control of Cardiac Output by Venous Return—The Frank-Starling Mechanism of the Heart | 245 | ||
| Cardiac Output is the Sum of All Tissue Blood Flows—Tissue Metabolism Regulates Most Local Blood Flow | 246 | ||
| Long-Term Cardiac Output Varies Inversely with Total Peripheral Resistance When Arterial Pressure Is Unchanged. | 246 | ||
| The Heart Has Limits for the Cardiac Output that It Can Achieve | 247 | ||
| Factors That Cause a Hypereffective Heart | 247 | ||
| Nervous Excitation Can Increase Heart Pumping. | 247 | ||
| Heart Hypertrophy Can Increase Pumping Effectiveness. | 247 | ||
| Factors That Cause a Hypoeffective Heart | 248 | ||
| Role of the Nervous System in Controlling Cardiac Output | 248 | ||
| Importance of the Nervous System in Maintaining Arterial Pressure When Peripheral Blood Vessels Are Dilated and Venous Return and Cardiac Output Increase. | 248 | ||
| Effect of the Nervous System to Increase the Arterial Pressure During Exercise. | 248 | ||
| Pathologically High or Low Cardiac Outputs | 248 | ||
| High Cardiac Output Caused by Reduced Total Peripheral Resistance | 248 | ||
| Low Cardiac Output | 249 | ||
| Decreased Cardiac Output Caused by Cardiac Factors. | 249 | ||
| Decrease in Cardiac Output Caused by Noncardiac Peripheral Factors—Decreased Venous Return. | 249 | ||
| A More Quantitative Analysis of Cardiac Output Regulation | 250 | ||
| Cardiac Output Curves Used in the Quantitative Analysis | 250 | ||
| Effect of External Pressure Outside the Heart on Cardiac Output Curves. | 250 | ||
| Combinations of Different Patterns of Cardiac Output Curves. | 251 | ||
| Venous Return Curves | 251 | ||
| Normal Venous Return Curve | 251 | ||
| Plateau in the Venous Return Curve at Negative Atrial Pressures Caused by Collapse of the Large Veins. | 252 | ||
| Mean Circulatory Filling Pressure, Mean Systemic Filling Pressure, and Their Effect on Venous Return | 252 | ||
| Effect of Blood Volume on Mean Circulatory Filling Pressure. | 252 | ||
| Sympathetic Nervous Stimulation Increases Mean Circulatory Filling Pressure. | 252 | ||
| Mean Systemic Filling Pressure and Its Relation to Mean Circulatory Filling Pressure. | 252 | ||
| Effect on the Venous Return Curve of Changes in Mean Systemic Filling Pressure. | 253 | ||
| When the “Pressure Gradient for Venous Return” Is Zero, There Is No Venous Return. | 253 | ||
| Resistance to Venous Return | 253 | ||
| Effect of Resistance to Venous Return on the Venous Return Curve. | 253 | ||
| Combinations of Venous Return Curve Patterns. | 254 | ||
| Analysis of Cardiac Output and Right Atrial Pressure Using Simultaneous Cardiac Output and Venous Return Curves | 254 | ||
| Effect of Increased Blood Volume on Cardiac Output. | 254 | ||
| Compensatory Effects Initiated in Response to Increased Blood Volume. | 255 | ||
| Effect of Sympathetic Stimulation on Cardiac Output. | 255 | ||
| Effect of Sympathetic Inhibition on Cardiac Output. | 255 | ||
| Effect of Opening a Large Arteriovenous Fistula. | 255 | ||
| Other Analyses of Cardiac Output Regulation. | 256 | ||
| Methods for Measuring Cardiac Output | 256 | ||
| Pulsatile Output of the Heart Measured by an Electromagnetic or Ultrasonic Flowmeter | 256 | ||
| Measurement of Cardiac Output Using the Oxygen Fick Principle | 256 | ||
| Indicator Dilution Method for Measuring Cardiac Output | 257 | ||
| Bibliography | 258 | ||
| 21 Muscle Blood Flow and Cardiac Output During Exercise; the Coronary Circulation and Ischemic Heart Disease | 259 | ||
| Blood Flow Regulation in Skeletal Muscle at Rest and During Exercise | 259 | ||
| Rate of Blood Flow through the Muscles | 259 | ||
| Blood Flow During Muscle Contractions. | 259 | ||
| Increased Blood Flow in Muscle Capillaries During Exercise. | 259 | ||
| Control of Blood Flow in Skeletal Muscles | 259 | ||
| Decreased Oxygen in Muscle Greatly Enhances Flow. | 259 | ||
| Nervous Control of Muscle Blood Flow. | 260 | ||
| Sympathetic Vasoconstrictor Nerves. | 260 | ||
| Circulatory Readjustments During Exercise | 260 | ||
| Effects of Sympathetic Activation | 260 | ||
| Sympathetic Stimulation May Increase Arterial Pressure During Exercise | 260 | ||
| Why Is Increased Arterial Pressure During Exercise Important? | 261 | ||
| Importance of the Increase in Cardiac Output During Exercise | 261 | ||
| Graphical Analysis of the Changes in Cardiac Output During Heavy Exercise. | 261 | ||
| Coronary Circulation | 262 | ||
| Physiologic Anatomy of the Coronary Blood Supply | 262 | ||
| Normal Coronary Blood Flow Averages Five Percent of Cardiac Output | 262 | ||
| Phasic Changes in Coronary Blood Flow During Systole and Diastole—Effect of Cardiac Muscle Compression. | 262 | ||
| Epicardial Versus Subendocardial Coronary Blood Flow—Effect of Intramyocardial Pressure. | 263 | ||
| Control of Coronary Blood Flow | 263 | ||
| Local Muscle Metabolism Is the Primary Controller of Coronary Flow | 263 | ||
| Oxygen Demand as a Major Factor in Local Coronary Blood Flow Regulation. | 263 | ||
| Nervous Control of Coronary Blood Flow | 263 | ||
| Direct Effects of Nervous Stimuli on the Coronary Vasculature. | 264 | ||
| Special Features of Cardiac Muscle Metabolism | 264 | ||
| Ischemic Heart Disease | 264 | ||
| Atherosclerosis as a Cause of Ischemic Heart Disease. | 264 | ||
| Acute Coronary Occlusion | 265 | ||
| Lifesaving Value of Collateral Circulation in the Heart. | 265 | ||
| Myocardial Infarction | 265 | ||
| Subendocardial Infarction. | 266 | ||
| Causes of Death After Acute Coronary Occlusion | 266 | ||
| Decreased Cardiac Output—Systolic Stretch and Cardiac Shock. | 266 | ||
| Damming of Blood in the Body’s Venous System. | 266 | ||
| Fibrillation of the Ventricles After Myocardial Infarction. | 267 | ||
| Rupture of the Infarcted Area. | 267 | ||
| Stages of Recovery from Acute Myocardial Infarction | 267 | ||
| Replacement of Dead Muscle by Scar Tissue. | 268 | ||
| Value of Rest in Treating Myocardial Infarction. | 268 | ||
| Function of the Heart After Recovery from Myocardial Infarction | 268 | ||
| Pain in Coronary Heart Disease | 268 | ||
| Angina Pectoris (Cardiac Pain). | 268 | ||
| Treatment with Drugs. | 269 | ||
| Surgical Treatment of Coronary Artery Disease | 269 | ||
| Aortic-Coronary Bypass Surgery. | 269 | ||
| Coronary Angioplasty. | 269 | ||
| Bibliography | 269 | ||
| 22 Cardiac Failure | 271 | ||
| Circulatory Dynamics in Cardiac Failure | 271 | ||
| Acute Effects of Moderate Cardiac Failure | 271 | ||
| Compensation for Acute Cardiac Failure by Sympathetic Nervous Reflexes. | 271 | ||
| Chronic Stage of Failure—Fluid Retention and Compensated Cardiac Output | 272 | ||
| Renal Retention of Fluid and Increase in Blood Volume Occur for Hours to Days | 272 | ||
| Moderate Fluid Retention in Cardiac Failure Can Be Beneficial. | 272 | ||
| Detrimental Effects of Excess Fluid Retention in Severe Cardiac Failure. | 272 | ||
| Recovery of the Heart After Myocardial Infarction | 272 | ||
| Cardiac Output Curve After Partial Recovery. | 273 | ||
| Summary of the Changes that Occur After Acute Cardiac Failure—“Compensated Heart Failure” | 273 | ||
| Compensated Heart Failure. | 273 | ||
| Dynamics of Severe Cardiac Failure—Decompensated Heart Failure | 273 | ||
| Graphical Analysis of Decompensated Heart Failure. | 273 | ||
| Treatment of Decompensation. | 274 | ||
| Mechanism of Action of the Cardiotonic Drugs Such as Digitalis. | 274 | ||
| Unilateral Left Heart Failure | 275 | ||
| Low-Output Cardiac Failure—Cardiogenic Shock | 275 | ||
| Vicious Cycle of Cardiac Deterioration in Cardiogenic Shock. | 275 | ||
| Physiology of Treatment. | 275 | ||
| Edema in Patients with Cardiac Failure | 275 | ||
| Acute Cardiac Failure Does Not Cause Immediate Peripheral Edema. | 275 | ||
| Long-Term Fluid Retention by the Kidneys Causes Peripheral Edema in Persisting Heart Failure | 276 | ||
| Role of Atrial Natriuretic Peptide in Delaying the Onset of Cardiac Decompensation. | 277 | ||
| Acute Pulmonary Edema in Late-Stage Heart Failure—Another Lethal Vicious Cycle | 277 | ||
| Cardiac Reserve | 277 | ||
| Diagnosis of Low Cardiac Reserve—Exercise Test. | 277 | ||
| Quantitative Graphical Method for Analysis of Cardiac Failure | 278 | ||
| Graphical Analysis of Acute Heart Failure and Chronic Compensation | 278 | ||
| Acute Heart Attack Reduces the Cardiac Output Curve. | 278 | ||
| Sympathetic Reflexes Raise Cardiac Output and Venous Return Curves. | 278 | ||
| Compensation During the Next Few Days Further Increases Cardiac Output and Venous Return Curves. | 278 | ||
| Graphical Analysis of “Decompensated” Cardiac Failure | 279 | ||
| Treatment of Decompensated Heart Disease with Digitalis. | 279 | ||
| Graphical Analysis of High-Output Cardiac Failure | 280 | ||
| Arteriovenous Fistula. | 280 | ||
| Beriberi. | 280 | ||
| Bibliography | 280 | ||
| 23 Heart Valves and Heart Sounds; Valvular and Congenital Heart Defects | 283 | ||
| Heart Sounds | 283 | ||
| Normal Heart Sounds | 283 | ||
| The First Heart Sound Is Associated with Closure of the A-V Valves. | 283 | ||
| The Second Heart Sound Is Associated with Closure of the Aortic and Pulmonary Valves. | 283 | ||
| Duration and Pitch of the First and Second Heart Sounds. | 283 | ||
| The Third Heart Sound Occurs at the Beginning of the Middle Third of Diastole. | 284 | ||
| Atrial Contraction Sound (Fourth Heart Sound). | 284 | ||
| Chest Surface Areas for Auscultation of Normal Heart Sounds. | 284 | ||
| Phonocardiogram. | 284 | ||
| Valvular Lesions | 285 | ||
| Rheumatic Valvular Lesions | 285 | ||
| Scarring of the Valves. | 285 | ||
| Other Causes of Valvular Lesions. | 285 | ||
| Heart Murmurs Are Caused by Valvular Lesions | 285 | ||
| Systolic Murmur of Aortic Stenosis. | 285 | ||
| Diastolic Murmur of Aortic Regurgitation. | 286 | ||
| Systolic Murmur of Mitral Regurgitation. | 286 | ||
| Diastolic Murmur of Mitral Stenosis. | 286 | ||
| Phonocardiograms of Valvular Murmurs. | 286 | ||
| Abnormal Circulatory Dynamics in Valvular Heart Disease | 286 | ||
| Dynamics of the Circulation in Aortic Stenosis and Aortic Regurgitation | 286 | ||
| Hypertrophy of the Left Ventricle. | 286 | ||
| Increase in Blood Volume. | 286 | ||
| Aortic Valvular Lesions May be Associated with Inadequate Coronary Blood Flow. | 287 | ||
| Eventual Failure of the Left Ventricle and Development of Pulmonary Edema. | 287 | ||
| Dynamics of Mitral Stenosis and Mitral Regurgitation | 287 | ||
| Pulmonary Edema in Mitral Valvular Disease. | 287 | ||
| Enlarged Left Atrium and Atrial Fibrillation. | 287 | ||
| Compensation in Early Mitral Valvular Disease. | 287 | ||
| Circulatory Dynamics during Exercise in Patients with Valvular Lesions | 287 | ||
| Abnormal Circulatory Dynamics in Congenital Heart Defects | 288 | ||
| Patent Ductus Arteriosus is a Left-to-Right Shunt | 288 | ||
| Closure of the Ductus Arteriosus After Birth. | 288 | ||
| Dynamics of the Circulation with a Persistent Patent Ductus | 289 | ||
| Recirculation Through the Lungs. | 289 | ||
| Diminished Cardiac and Respiratory Reserve. | 289 | ||
| Heart Sounds: Machinery Murmur | 289 | ||
| Surgical Treatment | 289 | ||
| Tetralogy of Fallot is a Right-to-Left Shunt | 289 | ||
| Abnormal Circulatory Dynamics. | 290 | ||
| Surgical Treatment. | 290 | ||
| Causes of Congenital Anomalies | 290 | ||
| Use of Extracorporeal Circulation during Cardiac Surgery | 290 | ||
| Hypertrophy of the Heart in Valvular and Congenital Heart Disease | 290 | ||
| Detrimental Effects of Late Stages of Cardiac Hypertrophy. | 290 | ||
| Bibliography | 291 | ||
| 24 Circulatory Shock and Its Treatment | 293 | ||
| Physiological Causes of Shock | 293 | ||
| Circulatory Shock Caused by Decreased Cardiac Output | 293 | ||
| Circulatory Shock Without Diminished Cardiac Output | 293 | ||
| What Happens to the Arterial Pressure in Circulatory Shock? | 293 | ||
| Tissue Deterioration is the End Result of Circulatory Shock | 293 | ||
| Stages of Shock | 294 | ||
| Shock Caused by Hypovolemia—Hemorrhagic Shock | 294 | ||
| Relationship of Bleeding Volume to Cardiac Output and Arterial Pressure | 294 | ||
| Sympathetic Reflex Compensations in Shock—Their Special Value to Maintain Arterial Pressure. | 294 | ||
| Value of the Sympathetic Nervous Reflexes. | 294 | ||
| Greater Effect of the Sympathetic Nervous Reflexes in Maintaining Arterial Pressure than in Maintaining Cardiac Output. | 294 | ||
| Protection of Coronary and Cerebral Blood Flow by the Reflexes. | 295 | ||
| Progressive and Nonprogressive Hemorrhagic Shock | 295 | ||
| Nonprogressive Shock—Compensated Shock | 295 | ||
| “Progressive Shock” Is Caused by a Vicious Cycle of Cardiovascular Deterioration | 296 | ||
| Cardiac Depression. | 296 | ||
| Vasomotor Failure. | 297 | ||
| Blockage of Very Small Vessels by “Sludged Blood.” | 297 | ||
| Increased Capillary Permeability. | 297 | ||
| Release of Toxins by Ischemic Tissue. | 297 | ||
| Cardiac Depression Caused by Endotoxin. | 297 | ||
| Generalized Cellular Deterioration. | 297 | ||
| Tissue Necrosis in Severe Shock—Patchy Areas of Necrosis Occur Because of Patchy Blood Flows in Different Organs. | 298 | ||
| Acidosis in Shock. | 298 | ||
| Positive Feedback Deterioration of Tissues in Shock and the Vicious Circle of Progressive Shock. | 298 | ||
| Irreversible Shock | 298 | ||
| Depletion of Cellular High-Energy Phosphate Reserves in Irreversible Shock. | 299 | ||
| Hypovolemic Shock Caused by Plasma Loss | 299 | ||
| Hypovolemic Shock Caused by Trauma | 299 | ||
| Neurogenic Shock—Increased Vascular Capacity | 299 | ||
| Causes of Neurogenic Shock. | 300 | ||
| Anaphylactic Shock and Histamine Shock | 300 | ||
| Septic Shock | 300 | ||
| Special Features of Septic Shock. | 300 | ||
| Physiology of Treatment in Shock | 301 | ||
| Replacement Therapy | 301 | ||
| Blood and Plasma Transfusion. | 301 | ||
| Dextran Solution as a Plasma Substitute. | 301 | ||
| Treatment of Neurogenic and Anaphylactic Shock with Sympathomimetic Drugs | 301 | ||
| Other Therapy | 301 | ||
| Treatment by the Head-Down Position. | 301 | ||
| Oxygen Therapy. | 302 | ||
| Treatment with Glucocorticoids. | 302 | ||
| Circulatory Arrest | 302 | ||
| Effect of Circulatory Arrest on the Brain | 302 | ||
| Bibliography | 302 | ||
| Unit V The Body Fluids and Kidneys | 303 | ||
| 25 The Body Fluid Compartments: | 305 | ||
| Fluid Intake and Output are Balanced during Steady-State Conditions | 305 | ||
| Daily Intake of Water | 305 | ||
| Daily Loss of Body Water | 305 | ||
| Insensible Water Loss. | 305 | ||
| Fluid Loss in Sweat. | 305 | ||
| Water Loss in Feces. | 305 | ||
| Water Loss by the Kidneys. | 305 | ||
| Body Fluid Compartments | 306 | ||
| Intracellular Fluid Compartment | 306 | ||
| Extracellular Fluid Compartment | 307 | ||
| Blood Volume | 307 | ||
| Hematocrit (Packed Red Blood Cell Volume). | 307 | ||
| Constituents of Extracellular and Intracellular Fluids | 307 | ||
| Ionic Composition of Plasma and Interstitial Fluid is Similar | 307 | ||
| Intracellular Fluid Constituents | 308 | ||
| Measurement of Fluid Volumes in the Different Body Fluid Compartments—the Indicator-Dilution Principle | 308 | ||
| Determination of Volumes of Specific Body Fluid Compartments | 309 | ||
| Measurement of Total Body Water. | 309 | ||
| Measurement of Extracellular Fluid Volume. | 309 | ||
| Calculation of Intracellular Volume. | 309 | ||
| Measurement of Plasma Volume. | 309 | ||
| Calculation of Interstitial Fluid Volume. | 310 | ||
| Measurement of Blood Volume. | 310 | ||
| Regulation of Fluid Exchange and Osmotic Equilibrium between Intracellular and Extracellular Fluid | 310 | ||
| Basic Principles of Osmosis and Osmotic Pressure | 310 | ||
| Osmolality and Osmolarity. | 310 | ||
| Calculation of the Osmolarity and Osmotic Pressure of a Solution. | 310 | ||
| Osmolarity of the Body Fluids. | 311 | ||
| Corrected Osmolar Activity of the Body Fluids. | 311 | ||
| Osmotic Equilibrium is Maintained between Intracellular and Extracellular Fluids | 311 | ||
| Isotonic, Hypotonic, and Hypertonic Fluids. | 311 | ||
| Isosmotic, Hyperosmotic, and Hypo-Osmotic Fluids. | 312 | ||
| Osmotic Equilibrium Between Intracellular and Extracellular Fluids Is Rapidly Attained. | 312 | ||
| Volume and Osmolality of Extracellular and Intracellular Fluids in Abnormal States | 312 | ||
| Effect of Adding Saline Solution to the Extracellular Fluid | 312 | ||
| Calculation of Fluid Shifts and Osmolarities After Infusion of Hypertonic Saline Solution. | 312 | ||
| Glucose and Other Solutions Administered for Nutritive Purposes | 314 | ||
| Clinical Abnormalities of Fluid Volume Regulation: Hyponatremia and Hypernatremia | 314 | ||
| Causes of Hyponatremia: Excess Water or Loss of Sodium | 314 | ||
| Consequences of Hyponatremia: Cell Swelling | 315 | ||
| Causes of Hypernatremia: Water Loss or Excess Sodium | 315 | ||
| Consequences of Hypernatremia: Cell Shrinkage | 316 | ||
| Edema: Excess Fluid in the Tissues | 316 | ||
| Intracellular Edema | 316 | ||
| Extracellular Edema | 316 | ||
| Factors That Can Increase Capillary Filtration | 316 | ||
| Lymphedema—Failure of the Lymph Vessels to Return Fluid and Protein to the Blood | 317 | ||
| Summary of Causes of Extracellular Edema | 317 | ||
| Edema Caused by Heart Failure. | 317 | ||
| Edema Caused by Decreased Kidney Excretion of Salt and Water. | 317 | ||
| Edema Caused by Decreased Plasma Proteins. | 318 | ||
| Safety Factors That Normally Prevent Edema | 318 | ||
| Safety Factor Caused by Low Compliance of the Interstitium in the Negative Pressure Range | 318 | ||
| Importance of Interstitial Gel in Preventing Fluid Accumulation in the Interstitium. | 319 | ||
| Importance of the Proteoglycan Filaments as a “Spacer” for the Cells and in Preventing Rapid Flow of Fluid in the Tissues. | 319 | ||
| Increased Lymph Flow as a Safety Factor Against Edema | 319 | ||
| “Washdown” of the Interstitial Fluid Protein as a Safety Factor Against Edema | 319 | ||
| Summary of Safety Factors That Prevent Edema | 320 | ||
| Fluids in the “Potential Spaces” of the Body | 320 | ||
| Fluid Is Exchanged Between the Capillaries and the Potential Spaces. | 320 | ||
| Lymphatic Vessels Drain Protein from the Potential Spaces. | 320 | ||
| Edema Fluid in the Potential Spaces Is Called Effusion. | 320 | ||
| Bibliography | 320 | ||
| 26 The Urinary System: | 323 | ||
| Multiple Functions of the Kidneys | 323 | ||
| Excretion of Metabolic Waste Products, Foreign Chemicals, Drugs, and Hormone Metabolites. | 323 | ||
| Regulation of Water and Electrolyte Balances. | 323 | ||
| Regulation of Arterial Pressure. | 324 | ||
| Regulation of Acid-Base Balance. | 324 | ||
| Regulation of Erythrocyte Production. | 324 | ||
| Regulation of 1,25-Dihydroxyvitamin D3 Production. | 324 | ||
| Glucose Synthesis. | 324 | ||
| Physiological Anatomy of the Kidneys | 324 | ||
| General Organization of the Kidneys and Urinary Tract | 324 | ||
| Renal Blood Supply | 325 | ||
| The Nephron is the Functional Unit of the Kidney | 325 | ||
| Regional Differences in Nephron Structure: Cortical and Juxtamedullary Nephrons. | 326 | ||
| Micturition | 327 | ||
| Physiological Anatomy of the Bladder | 327 | ||
| Innervation of the Bladder. | 328 | ||
| Transport of Urine From the Kidney Through the Ureters and Into the Bladder | 329 | ||
| Pain Sensation in the Ureters and the Ureterorenal Reflex. | 329 | ||
| Filling of the Bladder and Bladder Wall Tone; the Cystometrogram | 329 | ||
| Micturition Reflex | 330 | ||
| Facilitation or Inhibition of Micturition by the Brain. | 330 | ||
| Abnormalities of Micturition | 330 | ||
| Atonic Bladder and Incontinence Caused by Destruction of Sensory Nerve Fibers. | 330 | ||
| Automatic Bladder Caused by Spinal Cord Damage Above the Sacral Region. | 330 | ||
| Uninhibited Neurogenic Bladder Caused by Lack of Inhibitory Signals from the Brain. | 331 | ||
| Urine Formation Results From Glomerular Filtration, Tubular Reabsorption, and Tubular Secretion | 331 | ||
| Filtration, Reabsorption, and Secretion of Different Substances | 332 | ||
| Why Are Large Amounts of Solutes Filtered and Then Reabsorbed by the Kidneys? | 332 | ||
| Bibliography | 332 | ||
| 27 Glomerular Filtration, Renal Blood Flow, and Their Control | 335 | ||
| Glomerular Filtration—the First Step in Urine Formation | 335 | ||
| Composition of the Glomerular Filtrate | 335 | ||
| GFR is About 20 Percent of Renal Plasma Flow | 335 | ||
| Glomerular Capillary Membrane | 335 | ||
| Filterability of Solutes Is Inversely Related to Their Size. | 336 | ||
| Negatively Charged Large Molecules Are Filtered Less Easily Than Positively Charged Molecules of Equal Molecular Size. | 336 | ||
| Determinants of the GFR | 337 | ||
| Increased Glomerular Capillary Filtration Coefficient Increases GFR | 337 | ||
| Increased Bowman’s Capsule Hydrostatic Pressure Decreases GFR | 338 | ||
| Increased Glomerular Capillary Colloid Osmotic Pressure Decreases GFR | 338 | ||
| Increased Glomerular Capillary Hydrostatic Pressure Increases GFR | 339 | ||
| Renal Blood Flow | 340 | ||
| Renal Blood Flow and Oxygen Consumption | 340 | ||
| Determinants of Renal Blood Flow | 340 | ||
| Blood Flow in the Vasa Recta of the Renal Medulla is Very Low Compared with Flow in the Renal Cortex | 341 | ||
| Physiological Control of Glomerular Filtration and Renal Blood Flow | 341 | ||
| Strong Sympathetic Nervous System Activation Decreases GFR | 341 | ||
| Hormonal and Autacoid Control of Renal Circulation | 341 | ||
| Norepinephrine, Epinephrine, and Endothelin Constrict Renal Blood Vessels and Decrease GFR. | 341 | ||
| Angiotensin II Preferentially Constricts Efferent Arterioles in Most Physiological Conditions. | 342 | ||
| Endothelial-Derived Nitric Oxide Decreases Renal Vascular Resistance and Increases GFR. | 342 | ||
| Prostaglandins and Bradykinin Decrease Renal Vascular Resistance and Tend to Increase GFR. | 342 | ||
| Autoregulation of GFR and Renal Blood Flow | 342 | ||
| Importance of GFR Autoregulation in Preventing Extreme Changes in Renal Excretion | 343 | ||
| Tubuloglomerular Feedback and Autoregulation of GFR | 343 | ||
| Decreased Macula Densa Sodium Chloride Causes Dilation of Afferent Arterioles and Increased Renin Release. | 343 | ||
| Blockade of Angiotensin II Formation Further Reduces GFR During Renal Hypoperfusion. | 344 | ||
| Myogenic Autoregulation of Renal Blood Flow and GFR | 344 | ||
| Other Factors That Increase Renal Blood Flow and GFR: High Protein Intake and Increased Blood Glucose. | 345 | ||
| Bibliography | 346 | ||
| 28 Renal Tubular Reabsorption and Secretion | 347 | ||
| Tubular Reabsorption is Quantitatively Large and Highly Selective | 347 | ||
| Tubular Reabsorption Includes Passive and Active Mechanisms | 347 | ||
| Active Transport | 348 | ||
| Solutes Can Be Transported Through Epithelial Cells or Between Cells. | 348 | ||
| Primary Active Transport Through the Tubular Membrane Is Linked to Hydrolysis of ATP. | 348 | ||
| Secondary Active Reabsorption Through the Tubular Membrane. | 349 | ||
| Secondary Active Secretion into the Tubules. | 350 | ||
| Pinocytosis—An Active Transport Mechanism for Reabsorption of Proteins. | 350 | ||
| Transport Maximum for Substances That Are Actively Reabsorbed. | 350 | ||
| Transport Maximums for Substances That Are Actively Secreted. | 351 | ||
| Substances That Are Actively Transported but Do Not Exhibit a Transport Maximum. | 351 | ||
| Passive Water Reabsorption by Osmosis is Coupled Mainly to Sodium Reabsorption | 352 | ||
| Reabsorption of Chloride, Urea, and Other Solutes by Passive Diffusion | 352 | ||
| Reabsorption and Secretion Along Different Parts of the Nephron | 353 | ||
| Proximal Tubular Reabsorption | 353 | ||
| Proximal Tubules Have a High Capacity for Active and Passive Reabsorption. | 353 | ||
| Concentrations of Solutes Along the Proximal Tubule. | 354 | ||
| Secretion of Organic Acids and Bases by the Proximal Tubule. | 354 | ||
| Solute and Water Transport in the Loop of Henle | 354 | ||
| Distal Tubule | 355 | ||
| Late Distal Tubule and Cortical Collecting Tubule | 356 | ||
| Principal Cells Reabsorb Sodium and Secrete Potassium. | 356 | ||
| Intercalated Cells Secrete or Reabsorb Hydrogen, Bicarbonate, and Potassium Ions. | 357 | ||
| Medullary Collecting Duct | 358 | ||
| Summary of Concentrations of Different Solutes in the Different Tubular Segments | 358 | ||
| Tubular Fluid/Plasma Inulin Concentration Ratio Can Be Used to Measure Water Reabsorption by the Renal Tubules. | 359 | ||
| Regulation of Tubular Reabsorption | 359 | ||
| Glomerulotubular Balance—the Reabsorption Rate Increases in Response to Increased Tubular Load | 359 | ||
| Peritubular Capillary and Renal Interstitial Fluid Physical Forces | 360 | ||
| Normal Values for Physical Forces and Reabsorption Rate. | 360 | ||
| Regulation of Peritubular Capillary Physical Forces. | 360 | ||
| Renal Interstitial Hydrostatic and Colloid Osmotic Pressures. | 361 | ||
| Effect of Arterial Pressure on Urine Output—Pressure Natriuresis and Pressure Diuresis | 362 | ||
| Hormonal Control of Tubular Reabsorption | 362 | ||
| Aldosterone Increases Sodium Reabsorption and Potassium Secretion. | 363 | ||
| Angiotensin II Increases Sodium and Water Reabsorption. | 363 | ||
| ADH Increases Water Reabsorption. | 364 | ||
| Atrial Natriuretic Peptide Decreases Sodium and Water Reabsorption. | 364 | ||
| Parathyroid Hormone Increases Calcium Reabsorption. | 364 | ||
| Sympathetic Nervous System Activation Increases Sodium Reabsorption | 364 | ||
| Use of Clearance Methods to Quantify Kidney Function | 365 | ||
| Inulin Clearance Can be Used to Estimate GFR | 365 | ||
| Creatinine Clearance and Plasma Creatinine Concentration Can be Used to Estimate GFR | 366 | ||
| PAH Clearance Can be Used to Estimate RPF | 367 | ||
| Filtration Fraction is Calculated From GFR Divided by RPF | 368 | ||
| Calculation of Tubular Reabsorption or Secretion From Renal Clearances | 368 | ||
| Comparisons of Inulin Clearance with Clearances of Different Solutes. | 368 | ||
| Bibliography | 368 | ||
| 29 Urine Concentration and Dilution; Regulation of Extracellular Fluid Osmolarity and Sodium Concentration | 371 | ||
| Kidneys Excrete Excess Water by Forming Dilute Urine | 371 | ||
| Antidiuretic Hormone Controls Urine Concentration | 371 | ||
| Renal Mechanisms for Excreting Dilute Urine | 371 | ||
| Tubular Fluid Remains Isosmotic in the Proximal Tubule. | 372 | ||
| Tubular Fluid Is Diluted in the Ascending Loop of Henle. | 372 | ||
| Tubular Fluid in Distal and Collecting Tubules Is Further Diluted in the Absence of ADH. | 372 | ||
| Kidneys Conserve Water by Excreting Concentrated Urine | 373 | ||
| Obligatory Urine Volume | 373 | ||
| Urine Specific Gravity | 373 | ||
| Requirements for Excreting a Concentrated Urine—High ADH Levels and Hyperosmotic Renal Medulla | 374 | ||
| Countercurrent Multiplier Mechanism Produces a Hyperosmotic Renal Medullary Interstitium | 374 | ||
| Special Characteristics of the Loop of Henle That Cause Solutes to be Trapped in the Renal Medulla | 374 | ||
| Steps Involved in Causing Hyperosmotic Renal Medullary Interstitium. | 375 | ||
| Role of Distal Tubule and Collecting Ducts in Excreting Concentrated Urine | 376 | ||
| Urea Contributes to Hyperosmotic Renal Medullary Interstitium and Formation of Concentrated Urine | 376 | ||
| Recirculation of Urea from the Collecting Duct to the Loop of Henle Contributes to Hyperosmotic Renal Medulla. | 377 | ||
| Countercurrent Exchange in the Vasa Recta Preserves Hyperosmolarity of the Renal Medulla | 377 | ||
| Increased Medullary Blood Flow Reduces Urine-Concentrating Ability. | 378 | ||
| Summary of Urine-Concentrating Mechanism and Changes in Osmolarity in Different Segments of the Tubules | 378 | ||
| Proximal Tubule. | 378 | ||
| Descending Loop of Henle. | 378 | ||
| Thin Ascending Loop of Henle. | 379 | ||
| Thick Ascending Loop of Henle. | 379 | ||
| Early Distal Tubule. | 379 | ||
| Late Distal Tubule and Cortical Collecting Tubules. | 379 | ||
| Inner Medullary Collecting Ducts. | 379 | ||
| Quantifying Renal Urine Concentration And Dilution: “Free Water” and Osmolar Clearances | 380 | ||
| Relative Rates at Which Solutes and Water Are Excreted Can Be Assessed Using the Concept of “Free-Water Clearance” | 380 | ||
| Disorders of Urinary Concentrating Ability | 380 | ||
| Failure to Produce ADH: “Central” Diabetes Insipidus. | 380 | ||
| Inability of the Kidneys to Respond to ADH: “Nephrogenic” Diabetes Insipidus. | 381 | ||
| Control of Extracellular Fluid Osmolarity and Sodium Concentration | 381 | ||
| Estimating Plasma Osmolarity From Plasma Sodium Concentration | 381 | ||
| Osmoreceptor-ADH Feedback System | 381 | ||
| ADH Synthesis in Supraoptic and Paraventricular Nuclei of the Hypothalamus and ADH Release From the Posterior Pituitary | 382 | ||
| Stimulation of ADH Release by Decreased Arterial Pressure And/or Decreased Blood Volume | 383 | ||
| Quantitative Importance of Osmolarity and Cardiovascular Reflexes in Stimulating ADH Secretion | 383 | ||
| Other Stimuli for ADH Secretion | 384 | ||
| Importance of Thirst in Controlling Extracellular Fluid Osmolarity and Sodium Concentration | 384 | ||
| Central Nervous System Centers for Thirst | 384 | ||
| Stimuli for Thirst | 384 | ||
| Threshold for Osmolar Stimulus of Drinking | 385 | ||
| Integrated Responses of Osmoreceptor-ADH and Thirst Mechanisms in Controlling Extracellular Fluid Osmolarity and Sodium Concentration | 385 | ||
| Role of Angiotensin II and Aldosterone in Controlling Extracellular Fluid Osmolarity and Sodium Concentration | 385 | ||
| Salt-Appetite Mechanism for Controlling Extracellular Fluid Sodium Concentration and Volume | 386 | ||
| Bibliography | 387 | ||
| 30 Renal Regulation of Potassium, Calcium, Phosphate, and Magnesium; Integration of Renal Mechanisms for Control of Blood Volume and Extracellular Fluid Volume | 389 | ||
| Regulation of Extracellular Fluid Potassium Concentration and Potassium Excretion | 389 | ||
| Regulation of Internal Potassium Distribution | 389 | ||
| Insulin Stimulates Potassium Uptake into Cells. | 389 | ||
| Aldosterone Increases Potassium Uptake into Cells. | 389 | ||
| β-Adrenergic Stimulation Increases Cellular Uptake of Potassium. | 389 | ||
| Acid-Base Abnormalities Can Cause Changes in Potassium Distribution. | 390 | ||
| Cell Lysis Causes Increased Extracellular Potassium Concentration. | 390 | ||
| Strenuous Exercise Can Cause Hyperkalemia by Releasing Potassium from Skeletal Muscle. | 390 | ||
| Increased Extracellular Fluid Osmolarity Causes Redistribution of Potassium from the Cells to Extracellular Fluid. | 390 | ||
| Overview of Renal Potassium Excretion | 390 | ||
| Daily Variations in Potassium Excretion Are Caused Mainly by Changes in Potassium Secretion in Distal and Collecting Tubules. | 391 | ||
| Potassium Secretion by Principal Cells of Late Distal and Cortical Collecting Tubules | 391 | ||
| Control of Potassium Secretion by Principal Cells. | 392 | ||
| Intercalated Cells Can Reabsorb or Secrete Potassium. | 392 | ||
| Summary of Major Factors That Regulate Potassium Secretion | 392 | ||
| Increased Extracellular Fluid Potassium Concentration Stimulates Potassium Secretion. | 392 | ||
| Aldosterone Stimulates Potassium Secretion. | 393 | ||
| Increased Extracellular Potassium Ion Concentration Stimulates Aldosterone Secretion. | 393 | ||
| Blockade of the Aldosterone Feedback System Greatly Impairs Control of Potassium Concentration. | 393 | ||
| Increased Distal Tubular Flow Rate Stimulates Potassium Secretion. | 394 | ||
| Acute Acidosis Decreases Potassium Secretion. | 395 | ||
| Beneficial Effects of a Diet High in Potassium and Low in Sodium Content | 395 | ||
| Control of Renal Calcium Excretion and Extracellular Calcium Ion Concentration | 396 | ||
| Control of Calcium Excretion by the Kidneys | 396 | ||
| Proximal Tubular Calcium Reabsorption. | 397 | ||
| Loop of Henle and Distal Tubule Calcium Reabsorption. | 397 | ||
| Factors That Regulate Tubular Calcium Reabsorption. | 397 | ||
| Regulation of Renal Phosphate Excretion | 397 | ||
| Control of Renal Magnesium Excretion and Extracellular Magnesium Ion Concentration | 398 | ||
| Integration of Renal Mechanisms for Control of Extracellular Fluid | 398 | ||
| Sodium Intake and Excretion are Balanced Under Steady-State Conditions | 399 | ||
| Sodium Excretion is Controlled by Altering Glomerular Filtration or Tubular Sodium Reabsorption Rates | 399 | ||
| Importance of Pressure Natriuresis and Pressure Diuresis in Maintaining Body Sodium and Fluid Balance | 399 | ||
| Pressure Natriuresis and Diuresis are Key Components of a Renal–Body Fluid Feedback for Regulating Body Fluid Volumes and Arterial Pressure | 400 | ||
| Precision of Blood Volume and Extracellular Fluid Volume Regulation | 401 | ||
| Distribution of Extracellular Fluid between the Interstitial Spaces and Vascular System | 401 | ||
| Nervous and Hormonal Factors Increase the Effectiveness of Renal–Body Fluid Feedback Control | 402 | ||
| Sympathetic Nervous System Control of Renal Excretion: Arterial Baroreceptor and Low-Pressure Stretch Receptor Reflexes | 402 | ||
| Role of Ang II in Controlling Renal Excretion | 403 | ||
| Importance of Changes in Ang II in Altering Pressure Natriuresis. | 403 | ||
| Excessive Ang II Does Not Usually Cause Large Increases in Extracellular Fluid Volume Because Increased Arterial Pressure Counterbalances Ang II–Mediated Sodium Retention. | 403 | ||
| Role of Aldosterone in Controlling Renal Excretion | 404 | ||
| During Chronic Oversecretion of Aldosterone, the Kidneys “Escape” from Sodium Retention as Arterial Pressure Rises. | 404 | ||
| Role of ADH in Controlling Renal Water Excretion | 404 | ||
| Excess ADH Secretion Usually Causes Only Small Increases in Extracellular Fluid Volume but Large Decreases in Sodium Concentration. | 404 | ||
| Role of Atrial Natriuretic Peptide in Controlling Renal Excretion | 405 | ||
| Integrated Responses to Changes in Sodium Intake | 405 | ||
| High Sodium Intake Suppresses Antinatriuretic Systems and Activates Natriuretic Systems. | 405 | ||
| Conditions That Cause Large Increases in Blood Volume and Extracellular Fluid Volume | 405 | ||
| Increased Blood Volume and Extracellular Fluid Volume Caused by Heart Diseases | 405 | ||
| Increased Blood Volume Caused by Increased Capacity of Circulation | 406 | ||
| Conditions That Cause Large Increases in Extracellular Fluid Volume but with Normal Blood Volume | 406 | ||
| Nephrotic Syndrome—Loss of Plasma Proteins in Urine and Sodium Retention by the Kidneys | 406 | ||
| Liver Cirrhosis—Decreased Synthesis of Plasma Proteins by the Liver and Sodium Retention by the Kidneys | 406 | ||
| Bibliography | 407 | ||
| 31 Acid-Base Regulation | 409 | ||
| H+ Concentration is Precisely Regulated | 409 | ||
| Acids and Bases—Their Definitions and Meanings | 409 | ||
| Strong and Weak Acids and Bases. | 409 | ||
| Normal H+ Concentration and pH of Body Fluids and Changes That Occur in Acidosis and Alkalosis. | 409 | ||
| Defending Against Changes in H+ Concentration: Buffers, Lungs, and Kidneys | 410 | ||
| Buffering of H+ in the Body Fluids | 410 | ||
| Bicarbonate Buffer System | 411 | ||
| Quantitative Dynamics of the Bicarbonate Buffer System | 411 | ||
| Henderson-Hasselbalch Equation. | 412 | ||
| Bicarbonate Buffer System Titration Curve. | 412 | ||
| “Buffer Power” Is Determined by the Amount and Relative Concentrations of the Buffer Components. | 412 | ||
| The Bicarbonate Buffer System Is the Most Important Extracellular Buffer. | 413 | ||
| Phosphate Buffer System | 413 | ||
| Proteins are Important Intracellular Buffers | 413 | ||
| Isohydric Principle: All Buffers in a Common Solution Are in Equilibrium with the Same H+ Concentration | 414 | ||
| Respiratory Regulation of Acid-Base Balance | 414 | ||
| Pulmonary Expiration of CO2 Balances Metabolic Formation of CO2 | 414 | ||
| Increasing Alveolar Ventilation Decreases Extracellular Fluid H+ Concentration and Raises pH | 414 | ||
| Increased H+ Concentration Stimulates Alveolar Ventilation | 414 | ||
| Feedback Control of H+ Concentration by the Respiratory System. | 415 | ||
| Efficiency of Respiratory Control of H+ Concentration. | 415 | ||
| Buffering Power of the Respiratory System. | 415 | ||
| Impairment of Lung Function Can Cause Respiratory Acidosis. | 415 | ||
| Renal Control of Acid-Base Balance | 415 | ||
| Secretion of H+ and Reabsorption of HCO3− by the Renal Tubules | 416 | ||
| H+ is Secreted by Secondary Active Transport in the Early Tubular Segments | 416 | ||
| Filtered HCO3− is Reabsorbed by Interaction with H+ in the Tubules | 417 | ||
| HCO3− Is “Titrated” Against H+ in the Tubules. | 417 | ||
| Primary Active Secretion of H+ in the Intercalated Cells of Late Distal and Collecting Tubules | 417 | ||
| Combination of Excess H+ with Phosphate and Ammonia Buffers in the Tubule Generates “New” HCO3− | 418 | ||
| Phosphate Buffer System Carries Excess H+ Into the Urine and Generates New HCO3− | 418 | ||
| Excretion of Excess H+ and Generation of New HCO3− by the Ammonia Buffer System | 419 | ||
| Chronic Acidosis Increases NH4+ Excretion. | 420 | ||
| Quantifying Renal Acid-Base Excretion | 420 | ||
| Regulation of Renal Tubular H+ Secretion | 420 | ||
| Renal Correction of Acidosis—Increased Excretion of H+ and Addition of HCO3− to the Extracellular Fluid | 421 | ||
| Acidosis Decreases the HCO3−/H+ Ratio in Renal Tubular Fluid | 421 | ||
| Renal Correction of Alkalosis—Decreased Tubular Secretion of H+ and Increased Excretion of HCO3− | 422 | ||
| Alkalosis Increases the HCO3−/H+ Ratio in Renal Tubular Fluid | 422 | ||
| Clinical Causes of Acid-Base Disorders | 422 | ||
| Respiratory Acidosis Results from Decreased Ventilation and Increased Pco2 | 422 | ||
| Respiratory Alkalosis Results from Increased Ventilation and Decreased Pco2 | 423 | ||
| Metabolic Acidosis Results from Decreased Extracellular Fluid HCO3− Concentration | 423 | ||
| Renal Tubular Acidosis. | 423 | ||
| Diarrhea. | 423 | ||
| Vomiting of Intestinal Contents. | 423 | ||
| Diabetes Mellitus. | 423 | ||
| Ingestion of Acids. | 423 | ||
| Chronic Renal Failure. | 423 | ||
| Metabolic Alkalosis Results from Increased Extracellular Fluid HCO3− Concentration | 423 | ||
| Administration of Diuretics (Except the Carbonic Anhydrase Inhibitors). | 423 | ||
| Excess Aldosterone. | 424 | ||
| Vomiting of Gastric Contents. | 424 | ||
| Ingestion of Alkaline Drugs. | 424 | ||
| Treatment of Acidosis or Alkalosis | 424 | ||
| Clinical Measurements and Analysis of Acid-Base Disorders | 424 | ||
| Complex Acid-Base Disorders and Use of the Acid-Base Nomogram for Diagnosis | 425 | ||
| Use of Anion Gap to Diagnose Acid-Base Disorders | 426 | ||
| Bibliography | 426 | ||
| 32 Diuretics, Kidney Diseases | 427 | ||
| Diuretics and Their Mechanisms of Action | 427 | ||
| Osmotic Diuretics Decrease Water Reabsorption by Increasing the Osmotic Pressure of Tubular Fluid | 427 | ||
| “Loop” Diuretics Decrease Active Sodium-Chloride-Potassium Reabsorption in the Thick Ascending Loop of Henle | 427 | ||
| Thiazide Diuretics Inhibit Sodium-Chloride Reabsorption in the Early Distal Tubule | 428 | ||
| Carbonic Anhydrase Inhibitors Block Sodium Bicarbonate Reabsorption in the Proximal Tubules | 428 | ||
| Mineralocorticoid Receptor Antagonists Decrease Sodium Reabsorption From and Potassium Secretion Into the Collecting Tubules | 429 | ||
| Sodium Channel Blockers Decrease Sodium Reabsorption in the Collecting Tubules | 429 | ||
| Kidney Diseases | 429 | ||
| Acute Kidney Injury | 429 | ||
| Prerenal Acute Kidney Injury Caused by Decreased Blood Flow to the Kidney | 430 | ||
| Intrarenal Acute Kidney Injury Caused by Abnormalities Within the Kidney | 430 | ||
| Acute Kidney Injury Caused by Glomerulonephritis | 431 | ||
| Tubular Necrosis as a Cause of Acute Kidney Injury | 431 | ||
| Acute Tubular Necrosis Caused by Severe Renal Ischemia. | 431 | ||
| Acute Tubular Necrosis Caused by Toxins or Medications. | 431 | ||
| Postrenal Acute Kidney Injury Caused by Abnormalities of the Lower Urinary Tract | 431 | ||
| Physiological Effects of Acute Kidney Injury | 431 | ||
| Chronic Kidney Disease is Often Associated with Irreversible Loss of Functional Nephrons | 432 | ||
| Vicious Cycle of Chronic Kidney Disease Leading to End-Stage Renal Disease | 432 | ||
| Injury to the Renal Vasculature as a Cause of Chronic Kidney Disease | 433 | ||
| Injury to the Glomeruli as a Cause of Chronic Kidney Disease—Glomerulonephritis | 434 | ||
| Injury to the Renal Interstitium as a Cause of Chronic Kidney Disease—Interstitial Nephritis | 434 | ||
| Nephrotic Syndrome—Excretion of Protein in the Urine Because of Increased Glomerular Permeability | 434 | ||
| Nephron Function in Chronic Kidney Disease | 435 | ||
| Loss of Functional Nephrons Requires Surviving Nephrons to Excrete More Water and Solutes. | 435 | ||
| Isosthenuria—Inability of the Kidney to Concentrate or Dilute the Urine. | 436 | ||
| Effects of Renal Failure on the Body Fluids—Uremia | 436 | ||
| Water Retention and Development of Edema in Chronic Kidney Disease. | 437 | ||
| Increase in Urea and Other Nonprotein Nitrogens (Azotemia). | 437 | ||
| Acidosis in Chronic Kidney Disease. | 437 | ||
| Anemia in Chronic Kidney Disease Caused by Decreased Erythropoietin Secretion. | 437 | ||
| Osteomalacia in Chronic Kidney Disease Caused by Decreased Production of Active Vitamin D and by Phosphate Retention by the Kidneys. | 437 | ||
| Hypertension and Kidney Disease | 438 | ||
| Renal Lesions That Reduce the Ability of the Kidneys to Excrete Sodium and Water Promote Hypertension. | 438 | ||
| Hypertension Caused by Patchy Renal Damage and Increased Renal Secretion of Renin. | 438 | ||
| Kidney Diseases That Cause Loss of Entire Nephrons Lead to Chronic Kidney Disease but May Not Cause Hypertension | 438 | ||
| Specific Tubular Disorders | 439 | ||
| Renal Glycosuria—Failure of the Kidneys to Reabsorb Glucose. | 439 | ||
| Aminoaciduria—Failure of the Kidneys to Reabsorb Amino Acids. | 439 | ||
| Renal Hypophosphatemia—Failure of the Kidneys to Reabsorb Phosphate. | 439 | ||
| Renal Tubular Acidosis—Failure of the Tubules to Secrete Hydrogen Ions. | 439 | ||
| Nephrogenic Diabetes Insipidus—Failure of the Kidneys to Respond to Antidiuretic Hormone. | 439 | ||
| Fanconi’s Syndrome—A Generalized Reabsorptive Defect of the Renal Tubules. | 439 | ||
| Bartter’s Syndrome—Decreased Sodium, Chloride, and Potassium Reabsorption in the Loops of Henle. | 439 | ||
| Gitelman’s Syndrome—Decreased Sodium Chloride Reabsorption in the Distal Tubules. | 439 | ||
| Liddle’s Syndrome—Increased Sodium Reabsorption. | 440 | ||
| Treatment of Renal Failure by Transplantation or by Dialysis With an Artificial Kidney | 440 | ||
| Basic Principles of Dialysis | 440 | ||
| Dialyzing Fluid | 441 | ||
| Bibliography | 441 | ||
| Unit VI Blood Cells, Immunity, and Blood Coagulation | 443 | ||
| 33 Red Blood Cells, Anemia, and Polycythemia | 445 | ||
| Red Blood Cells (Erythrocytes) | 445 | ||
| Shape and Size of Red Blood Cells. | 445 | ||
| Concentration of Red Blood Cells in the Blood. | 445 | ||
| Quantity of Hemoglobin in the Cells. | 445 | ||
| Production of Red Blood Cells | 445 | ||
| Areas of the Body That Produce Red Blood Cells. | 445 | ||
| Genesis of Blood Cells | 446 | ||
| Pluripotential Hematopoietic Stem Cells, Growth Inducers, and Differentiation Inducers. | 446 | ||
| Stages of Differentiation of Red Blood Cells | 447 | ||
| Erythropoietin Regulates Red Blood Cell Production | 447 | ||
| Tissue Oxygenation Is the Most Essential Regulator of Red Blood Cell Production. | 448 | ||
| Erythropoietin Stimulates Red Blood Cell Production, and Its Formation Increases in Response to Hypoxia. | 448 | ||
| Erythropoietin Is Formed Mainly in the Kidneys. | 448 | ||
| Erythropoietin Stimulates Production of Proerythroblasts from Hematopoietic Stem Cells. | 448 | ||
| Maturation of Red Blood Cells Requires Vitamin B12 (Cyanocobalamin) and Folic Acid | 449 | ||
| Maturation Failure Caused by Poor Absorption of Vitamin B12 from the Gastrointestinal Tract—Pernicious Anemia. | 449 | ||
| Maturation Failure Caused by Folic Acid (Pteroylglutamic Acid) Deficiency. | 449 | ||
| Hemoglobin Formation | 449 | ||
| Hemoglobin Combines Reversibly With Oxygen. | 450 | ||
| Iron Metabolism | 450 | ||
| Transport and Storage of Iron. | 450 | ||
| Daily Loss of Iron. | 451 | ||
| Absorption of Iron from the Intestinal Tract | 451 | ||
| Regulation of Total Body Iron by Controlling Rate of Absorption. | 451 | ||
| The Life Span of Red Blood Cells is About 120 Days | 451 | ||
| Destruction of Hemoglobin by Macrophages. | 452 | ||
| Anemias | 452 | ||
| Blood Loss Anemia. | 452 | ||
| Aplastic Anemia Due to Bone Marrow Dysfunction. | 452 | ||
| Megaloblastic Anemia. | 452 | ||
| Hemolytic Anemia. | 452 | ||
| Effects of Anemia on Function of the Circulatory System | 453 | ||
| Polycythemia | 453 | ||
| Secondary Polycythemia. | 453 | ||
| Polycythemia Vera (Erythremia). | 453 | ||
| Effect of Polycythemia on Function of the Circulatory System | 453 | ||
| Bibliography | 453 | ||
| 34 Resistance of the Body to Infection: | 455 | ||
| Leukocytes (White Blood Cells) | 455 | ||
| General Characteristics of Leukocytes | 455 | ||
| Types of White Blood Cells. | 455 | ||
| Concentrations of the Different White Blood Cells in the Blood. | 455 | ||
| Genesis of White Blood Cells | 455 | ||
| Life Span of White Blood Cells | 456 | ||
| Neutrophils and Macrophages Defend Against Infections | 457 | ||
| White Blood Cells Enter the Tissue Spaces by Diapedesis. | 457 | ||
| White Blood Cells Move Through Tissue Spaces by Ameboid Motion. | 457 | ||
| White Blood Cells Are Attracted to Inflamed Tissue Areas by Chemotaxis. | 457 | ||
| Phagocytosis | 457 | ||
| Phagocytosis by Neutrophils. | 457 | ||
| Phagocytosis by Macrophages. | 458 | ||
| Once Phagocytized, Most Particles Are Digested by Intracellular Enzymes. | 458 | ||
| Neutrophils and Macrophages Can Kill Bacteria. | 458 | ||
| Monocyte-Macrophage Cell System (Reticuloendothelial System) | 458 | ||
| Tissue Macrophages in the Skin and Subcutaneous Tissues (Histiocytes). | 458 | ||
| Macrophages in the Lymph Nodes. | 458 | ||
| Alveolar Macrophages in the Lungs. | 459 | ||
| Macrophages (Kupffer Cells) in the Liver Sinusoids. | 459 | ||
| Macrophages of the Spleen and Bone Marrow. | 459 | ||
| Inflammation: Role of Neutrophils and Macrophages | 460 | ||
| Inflammation | 460 | ||
| “Walling-Off” Effect of Inflammation. | 460 | ||
| Macrophage and Neutrophil Responses during Inflammation | 460 | ||
| Tissue Macrophages Provide a First Line of Defense Against Infection. | 460 | ||
| Neutrophil Invasion of the Inflamed Area Is a Second Line of Defense. | 460 | ||
| Acute Increase in the Number of Neutrophils in the Blood—“Neutrophilia.” | 461 | ||
| Second Macrophage Invasion into the Inflamed Tissue Is a Third Line of Defense. | 461 | ||
| Increased Production of Granulocytes and Monocytes by the Bone Marrow Is a Fourth Line of Defense. | 461 | ||
| Feedback Control of the Macrophage and Neutrophil Responses | 461 | ||
| Formation of Pus | 462 | ||
| Eosinophils | 462 | ||
| Basophils | 462 | ||
| Leukopenia | 463 | ||
| Leukemias | 463 | ||
| Two General Types of Leukemia: Lymphocytic and Myelogenous. | 463 | ||
| Effects of Leukemia on the Body | 463 | ||
| Bibliography | 464 | ||
| 35 Resistance of the Body to Infection: | 465 | ||
| Acquired (Adaptive) Immunity | 465 | ||
| Basic Types of Acquired Immunity—Humoral and Cell Mediated | 465 | ||
| Both Types of Acquired Immunity are Initiated by Antigens | 465 | ||
| Lymphocytes are Responsible for Acquired Immunity | 466 | ||
| T and B Lymphocytes Promote “Cell-Mediated” Immunity or “Humoral” Immunity. | 466 | ||
| Preprocessing of the T and B Lymphocytes | 466 | ||
| The Thymus Gland Preprocesses the T Lymphocytes. | 466 | ||
| Liver and Bone Marrow Preprocess the B Lymphocytes. | 467 | ||
| T Lymphocytes and B-Lymphocyte Antibodies React Highly Specifically Against Specific Antigens—Role of Lymphocyte Clones | 467 | ||
| Millions of Specific Types of Lymphocytes Are Stored in the Lymphoid Tissue. | 467 | ||
| Origin of the Many Clones of Lymphocytes | 468 | ||
| Mechanism for Activating a Clone of Lymphocytes | 468 | ||
| Role of Macrophages in the Activation Process. | 468 | ||
| Role of the T Cells in Activation of the B Lymphocytes. | 468 | ||
| Specific Attributes of the B-Lymphocyte System—Humoral Immunity and the Antibodies | 469 | ||
| Formation of Antibodies by Plasma Cells. | 469 | ||
| Formation of “Memory” Cells Enhances the Antibody Response to Subsequent Antigen Exposure. | 469 | ||
| Nature of the Antibodies | 469 | ||
| Specificity of Antibodies. | 470 | ||
| Five General Classes of Antibodies. | 470 | ||
| Mechanisms of Action of Antibodies | 470 | ||
| Direct Action of Antibodies on Invading Agents. | 470 | ||
| Complement System for Antibody Action | 471 | ||
| Classical Pathway. | 471 | ||
| Special Attributes of the T-Lymphocyte System—Activated T Cells and Cell-Mediated Immunity | 472 | ||
| Release of Activated T Cells from Lymphoid Tissue and Formation of Memory Cells. | 472 | ||
| Antigen-Presenting Cells, MHC Proteins, and Antigen Receptors on the T Lymphocytes. | 472 | ||
| Several Types of T Cells and Their Different Functions | 472 | ||
| T-Helper Cells are the Most Numerous of the T Cells | 473 | ||
| Specific Regulatory Functions of the Lymphokines. | 473 | ||
| Stimulation of Growth and Proliferation of Cytotoxic T Cells and Suppressor T Cells. | 473 | ||
| Stimulation of B-Cell Growth and Differentiation to Form Plasma Cells and Antibodies. | 473 | ||
| Activation of the Macrophage System. | 473 | ||
| Feedback Stimulatory Effect on the T-Helper Cells. | 473 | ||
| Cytotoxic T Cells Are “Killer” Cells | 473 | ||
| Suppressor T Cells | 474 | ||
| Tolerance of the Acquired Immunity System to One’s Own Tissues—Role of Preprocessing in the Thymus and Bone Marrow | 474 | ||
| Most Tolerance Results from Clone Selection During Preprocessing. | 474 | ||
| Failure of the Tolerance Mechanism Causes Autoimmune Diseases. | 474 | ||
| Immunization by Injection of Antigens | 474 | ||
| Passive Immunity | 475 | ||
| Allergy and Hypersensitivity | 475 | ||
| Allergy Caused by Activated T Cells: Delayed-Reaction Allergy | 475 | ||
| “Atopic” Allergies Associated with Excess IgE Antibodies | 475 | ||
| Anaphylaxis. | 476 | ||
| Urticaria. | 476 | ||
| Hay Fever. | 476 | ||
| Asthma. | 476 | ||
| Bibliography | 476 | ||
| 36 Blood Types; Transfusion; Tissue and Organ Transplantation | 477 | ||
| Antigenicity Causes Immune Reactions of Blood | 477 | ||
| Multiplicity of Antigens in the Blood Cells | 477 | ||
| O-A-B Blood Types | 477 | ||
| A and B Antigens—Agglutinogens | 477 | ||
| Major O-A-B Blood Types. | 477 | ||
| Genetic Determination of the Agglutinogens. | 477 | ||
| Relative Frequencies of the Different Blood Types. | 478 | ||
| Agglutinins | 478 | ||
| Titer of the Agglutinins at Different Ages. | 478 | ||
| Origin of Agglutinins in the Plasma. | 478 | ||
| Agglutination Process in Transfusion Reactions | 478 | ||
| Acute Hemolysis Occurs in Some Transfusion Reactions. | 478 | ||
| Blood Typing | 479 | ||
| Rh Blood Types | 479 | ||
| Rh Antigens—“Rh-Positive” and “Rh-Negative” People. | 479 | ||
| Rh Immune Response | 479 | ||
| Formation of Anti-Rh Agglutinins. | 479 | ||
| Characteristics of Rh Transfusion Reactions. | 479 | ||
| Erythroblastosis Fetalis (“Hemolytic Disease of the Newborn”) | 479 | ||
| Incidence of the Disease. | 480 | ||
| Effect of the Mother’s Antibodies on the Fetus. | 480 | ||
| Clinical Picture of Erythroblastosis. | 480 | ||
| Treatment of Neonates with Erythroblastosis Fetalis. | 480 | ||
| Prevention of Erythroblastosis Fetalis. | 480 | ||
| Transfusion Reactions Resulting From Mismatched Blood Types | 480 | ||
| Acute Kidney Failure After Transfusion Reactions. | 480 | ||
| Transplantation of Tissues and Organs | 481 | ||
| Autografts, Isografts, Allografts, and Xenografts. | 481 | ||
| Transplantation of Cellular Tissues. | 481 | ||
| Attempts to Overcome Immune Reactions in Transplanted Tissue | 481 | ||
| Tissue Typing—The Human Leukocyte Antigen Complex of Antigens. | 481 | ||
| Prevention of Graft Rejection by Suppressing the Immune System | 481 | ||
| Bibliography | 482 | ||
| 37 Hemostasis and Blood Coagulation | 483 | ||
| Hemostasis Events | 483 | ||
| Vascular Constriction | 483 | ||
| Formation of the Platelet Plug | 483 | ||
| Physical and Chemical Characteristics of Platelets | 483 | ||
| Mechanism of the Platelet Plug | 484 | ||
| Importance of the Platelet Mechanism for Closing Vascular Holes. | 484 | ||
| Blood Coagulation in the Ruptured Vessel | 484 | ||
| Fibrous Organization or Dissolution of the Blood Clot | 485 | ||
| Mechanism of Blood Coagulation | 485 | ||
| General Mechanism | 485 | ||
| Conversion of Prothrombin to Thrombin | 485 | ||
| Prothrombin and Thrombin. | 485 | ||
| Conversion of Fibrinogen to Fibrin—Formation of the Clot | 486 | ||
| Fibrinogen Formed in the Liver Is Essential for Clot Formation. | 486 | ||
| Action of Thrombin on Fibrinogen to Form Fibrin. | 486 | ||
| Blood Clot. | 486 | ||
| Clot Retraction and Expression of Serum. | 486 | ||
| Positive Feedback of Clot Formation | 486 | ||
| Initiation of Coagulation: Formation of Prothrombin Activator | 487 | ||
| Extrinsic Pathway for Initiating Clotting | 487 | ||
| Intrinsic Pathway for Initiating Clotting | 487 | ||
| Role of Calcium Ions in the Intrinsic and Extrinsic Pathways | 488 | ||
| Interaction between the Extrinsic and Intrinsic Pathways—Summary of Blood-Clotting Initiation | 489 | ||
| Intravascular Anticoagulants Prevent Blood Clotting in the Normal Vascular System | 489 | ||
| Endothelial Surface Factors. | 489 | ||
| Antithrombin Action of Fibrin and Antithrombin III. | 489 | ||
| Heparin. | 489 | ||
| Plasmin Causes Lysis of Blood Clots | 489 | ||
| Activation of Plasminogen to Form Plasmin, Then Lysis of Clots. | 490 | ||
| Conditions That Cause Excessive Bleeding in Humans | 490 | ||
| Decreased Prothrombin, Factor VII, Factor IX, and Factor X Caused by Vitamin K Deficiency | 490 | ||
| Hemophilia | 490 | ||
| Thrombocytopenia | 491 | ||
| Thromboembolic Conditions | 491 | ||
| Thrombi and Emboli. | 491 | ||
| Cause of Thromboembolic Conditions. | 491 | ||
| Use of t-PA in Treating Intravascular Clots. | 491 | ||
| Femoral Venous Thrombosis and Massive Pulmonary Embolism | 491 | ||
| Disseminated Intravascular Coagulation | 491 | ||
| Anticoagulants for Clinical Use | 492 | ||
| Heparin as an Intravenous Anticoagulant | 492 | ||
| Coumarins as Anticoagulants | 492 | ||
| Prevention of Blood Coagulation Outside the Body | 492 | ||
| Blood Coagulation Tests | 493 | ||
| Bleeding Time | 493 | ||
| Clotting Time | 493 | ||
| Prothrombin Time and International Normalized Ratio | 493 | ||
| Bibliography | 493 | ||
| Unit VII Respiration | 495 | ||
| 38 Pulmonary Ventilation | 497 | ||
| Mechanics of Pulmonary Ventilation | 497 | ||
| Muscles That Cause Lung Expansion and Contraction | 497 | ||
| Pressures That Cause the Movement of Air in and out of the Lungs | 497 | ||
| Pleural Pressure and Its Changes during Respiration. | 498 | ||
| Alveolar Pressure—The Air Pressure Inside the Lung Alveoli. | 498 | ||
| Transpulmonary Pressure—The Difference between Alveolar and Pleural Pressures. | 499 | ||
| Compliance of the Lungs | 499 | ||
| Compliance Diagram of the Lungs. | 499 | ||
| Surfactant, Surface Tension, and Collapse of the Alveoli | 499 | ||
| Principle of Surface Tension. | 499 | ||
| Surfactant and Its Effect on Surface Tension. | 500 | ||
| Pressure in Occluded Alveoli Caused by Surface Tension. | 500 | ||
| Effect of Alveolar Radius on the Pressure Caused by Surface Tension. | 500 | ||
| Effect of the Thoracic Cage on Lung Expansibility | 500 | ||
| Compliance of the Thorax and the Lungs Together | 500 | ||
| “Work” of Breathing | 500 | ||
| Energy Required for Respiration. | 501 | ||
| Pulmonary Volumes and Capacities | 501 | ||
| Recording Changes in Pulmonary Volume—Spirometry | 501 | ||
| Pulmonary Volumes | 501 | ||
| Pulmonary Capacities | 501 | ||
| Abbreviations and Symbols Used in Pulmonary Function Studies | 502 | ||
| Determination of Functional Residual Capacity, Residual Volume, and Total Lung Capacity—Helium Dilution Method | 502 | ||
| Minute Respiratory Volume Equals Respiratory Rate Times Tidal Volume | 503 | ||
| Alveolar Ventilation | 503 | ||
| “Dead Space” and Its Effect on Alveolar Ventilation | 503 | ||
| Measurement of the Dead Space Volume. | 503 | ||
| Normal Dead Space Volume. | 504 | ||
| Anatomical Versus Physiological Dead Space. | 504 | ||
| Rate of Alveolar Ventilation | 504 | ||
| Functions of the Respiratory Passageways | 504 | ||
| Trachea, Bronchi, and Bronchioles | 504 | ||
| Muscular Wall of the Bronchi and Bronchioles and Its Control. | 504 | ||
| Resistance to Airflow in the Bronchial Tree. | 504 | ||
| Nervous and Local Control of the Bronchiolar Musculature—“Sympathetic” Dilation of the Bronchioles. | 505 | ||
| Parasympathetic Constriction of the Bronchioles. | 505 | ||
| Local Secretory Factors May Cause Bronchiolar Constriction. | 505 | ||
| Mucus Lining the Respiratory Passageways, and Action of Cilia to Clear the Passageways | 505 | ||
| Cough Reflex | 506 | ||
| Sneeze Reflex | 506 | ||
| Normal Respiratory Functions of the Nose | 506 | ||
| Filtration Function of the Nose. | 506 | ||
| Size of Particles Entrapped in the Respiratory Passages. | 506 | ||
| Vocalization | 506 | ||
| Phonation. | 507 | ||
| Articulation and Resonance. | 507 | ||
| Bibliography | 507 | ||
| 39 Pulmonary Circulation, Pulmonary Edema, Pleural Fluid | 509 | ||
| Physiological Anatomy of the Pulmonary Circulatory System | 509 | ||
| Pulmonary Vessels. | 509 | ||
| Bronchial Vessels. | 509 | ||
| Lymphatics. | 509 | ||
| Pressures in the Pulmonary System | 509 | ||
| Pressures in the Right Ventricle. | 509 | ||
| Pressures in the Pulmonary Artery. | 509 | ||
| Pulmonary Capillary Pressure. | 510 | ||
| Left Atrial and Pulmonary Venous Pressures. | 510 | ||
| Blood Volume of the Lungs | 510 | ||
| The Lungs Serve as a Blood Reservoir. | 510 | ||
| Cardiac Pathology May Shift Blood From the Systemic Circulation to the Pulmonary Circulation. | 510 | ||
| Blood Flow Through the Lungs and Its Distribution | 510 | ||
| Decreased Alveolar Oxygen Reduces Local Alveolar Blood Flow and Regulates Pulmonary Blood Flow Distribution. | 511 | ||
| Effect of Hydrostatic Pressure Gradients in the Lungs on Regional Pulmonary Blood Flow | 511 | ||
| Zones 1, 2, and 3 of Pulmonary Blood Flow | 511 | ||
| Zone 1 Blood Flow Occurs Only Under Abnormal Conditions. | 512 | ||
| Exercise Increases Blood Flow Through All Parts of the Lungs. | 512 | ||
| Increased Cardiac Output during Heavy Exercise is Normally Accommodated by the Pulmonary Circulation Without Large Increases in Pulmonary Artery Pressure | 512 | ||
| Function of the Pulmonary Circulation When the Left Atrial Pressure Rises as a Result of Left-Sided Heart Failure | 513 | ||
| Pulmonary Capillary Dynamics | 513 | ||
| Pulmonary Capillary Pressure. | 513 | ||
| Length of Time Blood Stays in the Pulmonary Capillaries. | 513 | ||
| Capillary Exchange of Fluid in the Lungs and Pulmonary Interstitial Fluid Dynamics | 513 | ||
| Interrelations Between Interstitial Fluid Pressure and Other Pressures in the Lung. | 514 | ||
| Negative Pulmonary Interstitial Pressure and the Mechanism for Keeping the Alveoli “Dry.” | 514 | ||
| Pulmonary Edema | 514 | ||
| “Pulmonary Edema Safety Factor.” | 514 | ||
| Safety Factor in Chronic Conditions. | 515 | ||
| Rapidity of Death in Persons with Acute Pulmonary Edema. | 515 | ||
| Fluid in the Pleural Cavity | 515 | ||
| “Negative Pressure” in Pleural Fluid. | 515 | ||
| Pleural Effusion—Collection of Large Amounts of Free Fluid in the Pleural Space. | 515 | ||
| Bibliography | 516 | ||
| 40 Principles of Gas Exchange; Diffusion of Oxygen and Carbon Dioxide Through the Respiratory Membrane | 517 | ||
| Physics of Gas Diffusion and Gas Partial Pressures | 517 | ||
| Molecular Basis of Gas Diffusion | 517 | ||
| Net Diffusion of a Gas in One Direction—Effect of a Concentration Gradient. | 517 | ||
| Gas Pressures in a Mixture of Gases—“Partial Pressures” of Individual Gases | 517 | ||
| Pressures of Gases Dissolved in Water and Tissues | 517 | ||
| Factors That Determine the Partial Pressure of a Gas Dissolved in a Fluid. | 517 | ||
| Diffusion of Gases Between the Gas Phase in the Alveoli and the Dissolved Phase in the Pulmonary Blood. | 518 | ||
| Vapor Pressure of Water | 518 | ||
| Pressure Difference Causes Net Diffusion of Gases Through Fluids | 518 | ||
| Quantifying the Net Rate of Diffusion in Fluids. | 518 | ||
| Diffusion of Gases Through Tissues | 519 | ||
| Compositions of Alveolar Air and Atmospheric Air are Different | 519 | ||
| Humidification of the Air in the Respiratory Passages | 519 | ||
| Alveolar Air is Slowly Renewed by Atmospheric Air | 519 | ||
| Importance of the Slow Replacement of Alveolar Air. | 520 | ||
| Oxygen Concentration and Partial Pressure in the Alveoli | 520 | ||
| CO2 Concentration and Partial Pressure in the Alveoli | 521 | ||
| Expired Air Is a Combination of Dead Space Air and Alveolar Air | 521 | ||
| Diffusion of Gases Through the Respiratory Membrane | 521 | ||
| Respiratory Unit. | 521 | ||
| Respiratory Membrane. | 521 | ||
| Factors That Affect the Rate of Gas Diffusion Through the Respiratory Membrane | 522 | ||
| Diffusing Capacity of the Respiratory Membrane | 523 | ||
| Diffusing Capacity for Oxygen. | 523 | ||
| Increased Oxygen Diffusing Capacity during Exercise. | 523 | ||
| Diffusing Capacity for Carbon Dioxide. | 524 | ||
| Measurement of Diffusing Capacity—The Carbon Monoxide Method. | 524 | ||
| Effect of the Ventilation-Perfusion Ratio on Alveolar Gas Concentration | 524 | ||
| Alveolar Oxygen and Carbon Dioxide Partial Pressures When Equals Zero. | 525 | ||
| Alveolar Oxygen and Carbon Dioxide Partial Pressures When Equals Infinity. | 525 | ||
| Gas Exchange and Alveolar Partial Pressures When Is Normal. | 525 | ||
| Po2-Pco2, Diagram | 525 | ||
| Concept of “Physiological Shunt” (When Is Below Normal) | 525 | ||
| Concept of the “Physiological Dead Space” (When Is Greater Than Normal) | 526 | ||
| Abnormalities of Ventilation-Perfusion Ratio | 526 | ||
| Abnormal in the Upper and Lower Normal Lung. | 526 | ||
| Abnormal in Chronic Obstructive Lung Disease. | 526 | ||
| Bibliography | 526 | ||
| 41 Transport of Oxygen and Carbon Dioxide in Blood and Tissue Fluids | 527 | ||
| Transport of Oxygen From the Lungs to the Body Tissues | 527 | ||
| Diffusion of Oxygen From the Alveoli to the Pulmonary Capillary Blood | 527 | ||
| Uptake of Oxygen by the Pulmonary Blood during Exercise. | 527 | ||
| Transport of Oxygen in the Arterial Blood | 528 | ||
| Diffusion of Oxygen From the Peripheral Capillaries Into the Tissue Fluid | 528 | ||
| Increasing Blood Flow Raises Interstitial Fluid Po2. | 528 | ||
| Increasing Tissue Metabolism Decreases Interstitial Fluid Po2. | 528 | ||
| Diffusion of Oxygen From the Peripheral Capillaries to the Tissue Cells | 529 | ||
| Diffusion of Carbon Dioxide From Peripheral Tissue Cells Into the Capillaries and From the Pulmonary Capillaries Into Alveoli | 529 | ||
| Effect of Rate of Tissue Metabolism and Tissue Blood Flow on Interstitial Pco2. | 529 | ||
| Role of Hemoglobin in Oxygen Transport | 530 | ||
| Reversible Combination of O2 with Hemoglobin | 530 | ||
| Oxygen-Hemoglobin Dissociation Curve. | 530 | ||
| Maximum Amount of Oxygen That Can Combine with the Hemoglobin of the Blood. | 530 | ||
| Amount of Oxygen Released From the Hemoglobin When Systemic Arterial Blood Flows Through the Tissues. | 530 | ||
| Transport of Oxygen Is Markedly Increased during Strenuous Exercise. | 531 | ||
| Utilization Coefficient. | 531 | ||
| Hemoglobin “Buffers” Tissue Po2 | 531 | ||
| Hemoglobin Helps Maintain Nearly Constant Po2 in the Tissues. | 531 | ||
| When Atmospheric Oxygen Concentration Changes Markedly, the Buffer Effect of Hemoglobin Still Maintains Almost Constant Tissue Po2. | 531 | ||
| Factors That Shift the Oxygen-Hemoglobin Dissociation Curve—Their Importance for Oxygen Transport | 532 | ||
| Increased Delivery of Oxygen to the Tissues When Carbon Dioxide and Hydrogen Ions Shift the Oxygen-Hemoglobin Dissociation Curve—the Bohr Effect | 532 | ||
| Effect of BPG to Cause Rightward Shift of the Oxygen-Hemoglobin Dissociation Curve | 532 | ||
| Rightward Shift of the Oxygen-Hemoglobin Dissociation Curve during Exercise | 532 | ||
| Metabolic Use of Oxygen by the Cells | 533 | ||
| Effect of Intracellular Po2 on Rate of Oxygen Usage. | 533 | ||
| Effect of Diffusion Distance From the Capillary to the Cell on Oxygen Usage. | 533 | ||
| Effect of Blood Flow on Metabolic Use of Oxygen. | 533 | ||
| Transport of Oxygen in the Dissolved State | 533 | ||
| Combination of Hemoglobin with Carbon Monoxide—Displacement of O2 | 534 | ||
| Transport of Carbon Dioxide in the Blood | 534 | ||
| Chemical Forms in Which Carbon Dioxide is Transported | 534 | ||
| Transport of Carbon Dioxide in the Dissolved State | 534 | ||
| Transport of Carbon Dioxide in the Form of Bicarbonate Ion | 535 | ||
| Reaction of Carbon Dioxide with Water in the Red Blood Cells—Effect of Carbonic Anhydrase. | 535 | ||
| Dissociation of Carbonic Acid Into Bicarbonate and Hydrogen Ions. | 535 | ||
| Transport of Carbon Dioxide in Combination with Hemoglobin and Plasma Proteins—Carbaminohemoglobin. | 535 | ||
| Carbon Dioxide Dissociation Curve | 535 | ||
| When Oxygen Binds with Hemoglobin, Carbon Dioxide is Released (the Haldane Effect) to Increase Carbon Dioxide Transport | 535 | ||
| Change in Blood Acidity During CO2 Transport | 536 | ||
| Respiratory Exchange Ratio | 536 | ||
| Bibliography | 536 | ||
| 42 Regulation of Respiration | 539 | ||
| Respiratory Center | 539 | ||
| Dorsal Respiratory Group of Neurons—Its Control of Inspiration and Respiratory Rhythm | 539 | ||
| Rhythmical Inspiratory Discharges From the Dorsal Respiratory Group. | 539 | ||
| Inspiratory “Ramp” Signal. | 539 | ||
| A Pneumotaxic Center Limits the Duration of Inspiration and Increases the Respiratory Rate | 540 | ||
| Ventral Respiratory Group of Neurons—Functions in Both Inspiration and Expiration | 540 | ||
| Lung Inflation Signals Limit Inspiration—the Hering-Breuer Inflation Reflex | 540 | ||
| Control of Overall Respiratory Center Activity | 540 | ||
| Chemical Control of Respiration | 541 | ||
| Direct Chemical Control of Respiratory Center Activity by CO2 and Hydrogen Ions | 541 | ||
| Chemosensitive Area of the Respiratory Center Beneath the Ventral Surface of the Medulla. | 541 | ||
| Excitation of the Chemosensitive Neurons by Hydrogen Ions Is Likely the Primary Stimulus | 541 | ||
| CO2 Stimulates the Chemosensitive Area | 541 | ||
| Decreased Stimulatory Effect of CO2 After the First 1 to 2 Days. | 541 | ||
| Quantitative Effects of Blood Pco2 and Hydrogen Ion Concentration on Alveolar Ventilation | 542 | ||
| Changes in O2 Have Little Direct Effect on Control of the Respiratory Center | 542 | ||
| Peripheral Chemoreceptor System for Control of Respiratory Activity—Role of Oxygen in Respiratory Control | 542 | ||
| Decreased Arterial Oxygen Stimulates the Chemoreceptors. | 543 | ||
| Increased Carbon Dioxide and Hydrogen Ion Concentration Stimulates the Chemoreceptors. | 543 | ||
| Basic Mechanism of Stimulation of the Chemoreceptors by O2 Deficiency. | 543 | ||
| Effect of Low Arterial Po2 to Stimulate Alveolar Ventilation When Arterial CO2 and Hydrogen Ion Concentrations Remain Normal | 543 | ||
| Chronic Breathing of Low O2 Stimulates Respiration Even More—The Phenomenon of “Acclimatization” | 544 | ||
| Composite Effects of Pco2, pH, and Po2 on Alveolar Ventilation | 544 | ||
| Regulation of Respiration during Exercise | 545 | ||
| Interrelation Between Chemical Factors and Nervous Factors in the Control of Respiration during Exercise. | 545 | ||
| Neurogenic Control of Ventilation During Exercise May Be Partly a Learned Response. | 546 | ||
| Other Factors That Affect Respiration | 546 | ||
| Voluntary Control of Respiration. | 546 | ||
| Effect of Irritant Receptors in the Airways. | 546 | ||
| Function of Lung “J Receptors.” | 546 | ||
| Brain Edema Depresses the Respiratory Center. | 546 | ||
| Anesthesia. | 546 | ||
| Periodic Breathing. | 546 | ||
| Basic Mechanism of Cheyne-Stokes Breathing. | 547 | ||
| Sleep Apnea | 547 | ||
| Obstructive Sleep Apnea Is Caused by Blockage of the Upper Airway. | 547 | ||
| “Central” Sleep Apnea Occurs When the Neural Drive to Respiratory Muscles Is Transiently Abolished. | 548 | ||
| Bibliography | 548 | ||
| 43 Respiratory Insufficiency—Pathophysiology, Diagnosis, Oxygen Therapy | 549 | ||
| Useful Methods for Studying Respiratory Abnormalities | 549 | ||
| Study of Blood Gases and Blood pH | 549 | ||
| Determination of Blood pH. | 549 | ||
| Determination of Blood CO2. | 549 | ||
| Determination of Blood PO2. | 549 | ||
| Measurement of Maximum Expiratory Flow | 550 | ||
| Abnormalities of the Maximum Expiratory Flow-Volume Curve. | 550 | ||
| Forced Expiratory Vital Capacity and Forced Expiratory Volume | 551 | ||
| Pathophysiology of Specific Pulmonary Abnormalities | 551 | ||
| Chronic Pulmonary Emphysema | 551 | ||
| Pneumonia—Lung Inflammation and Fluid in Alveoli | 552 | ||
| Atelectasis—Collapse of the Alveoli | 553 | ||
| Airway Obstruction Causes Lung Collapse. | 553 | ||
| Lack of “Surfactant” as a Cause of Lung Collapse. | 553 | ||
| Asthma—Spasmodic Contraction of Smooth Muscles in Bronchioles | 554 | ||
| Tuberculosis | 554 | ||
| Hypoxia and Oxygen Therapy | 554 | ||
| Inadequate Tissue Capability to Use Oxygen. | 555 | ||
| Effects of Hypoxia on the Body. | 555 | ||
| Oxygen Therapy in Different Types of Hypoxia | 555 | ||
| Cyanosis | 555 | ||
| Hypercapnia—Excess Carbon Dioxide in the Body Fluids | 556 | ||
| Dyspnea | 556 | ||
| Artificial Respiration | 556 | ||
| Resuscitator. | 556 | ||
| Tank Respirator (the “Iron Lung”). | 556 | ||
| Effect of the Resuscitator and the Tank Respirator on Venous Return. | 557 | ||
| Bibliography | 557 | ||
| Unit VIII Aviation, Space, and Deep–Sea Diving Physiology | 559 | ||
| 44 Aviation, High Altitude, and Space Physiology | 561 | ||
| Effects of Low Oxygen Pressure on the Body | 561 | ||
| Barometric Pressures at Different Altitudes. | 561 | ||
| Alveolar Po2 at Different Elevations | 561 | ||
| Carbon Dioxide and Water Vapor Decrease the Alveolar Oxygen. | 561 | ||
| Alveolar Po2 at Different Altitudes. | 561 | ||
| Saturation of Hemoglobin with Oxygen at Different Altitudes. | 561 | ||
| Effect of Breathing Pure Oxygen on Alveolar Po2 at Different Altitudes | 562 | ||
| The “Ceiling” When Breathing Air and When Breathing Oxygen in an Unpressurized Airplane. | 562 | ||
| Acute Effects of Hypoxia | 562 | ||
| Acclimatization to Low Po2 | 562 | ||
| Increased Pulmonary Ventilation—Role of Arterial Chemoreceptors. | 563 | ||
| Increase in Red Blood Cells and Hemoglobin Concentration During Acclimatization. | 563 | ||
| Increased Diffusing Capacity After Acclimatization. | 563 | ||
| Peripheral Circulatory System Changes During Acclimatization—Increased Tissue Capillarity. | 563 | ||
| Cellular Acclimatization. | 563 | ||
| Hypoxia-Inducible Factors—a “Master Switch” for the Body’s Response to Hypoxia | 563 | ||
| Natural Acclimatization of Native Human Beings Living at High Altitudes | 564 | ||
| Reduced Work Capacity at High Altitudes and Positive Effect of Acclimatization | 564 | ||
| Acute Mountain Sickness and High-Altitude Pulmonary Edema | 564 | ||
| Chronic Mountain Sickness | 565 | ||
| Effects of Acceleratory Forces on the Body in Aviation and Space Physiology | 565 | ||
| Centrifugal Acceleratory Forces | 565 | ||
| Measurement of Acceleratory Force—“G.” | 565 | ||
| Effects of Centrifugal Acceleratory Force on the Body (Positive G) | 565 | ||
| Effects on the Circulatory System. | 565 | ||
| Effects on the Vertebrae. | 566 | ||
| Negative G. | 566 | ||
| Protection of the Body Against Centrifugal Acceleratory Forces. | 566 | ||
| Effects of Linear Acceleratory Forces on the Body | 566 | ||
| Acceleratory Forces in Space Travel. | 566 | ||
| Deceleratory Forces Associated with Parachute Jumps. | 567 | ||
| “Artificial Climate” in the Sealed Spacecraft | 567 | ||
| Weightlessness in Space | 567 | ||
| Physiological Challenges of Weightlessness (Microgravity). | 567 | ||
| Cardiovascular, Muscle, and Bone “Deconditioning” During Prolonged Exposure to Weightlessness. | 568 | ||
| Bibliography | 568 | ||
| 45 Physiology of Deep-Sea Diving and Other Hyperbaric Conditions | 569 | ||
| Relationship of Pressure to Sea Depth. | 569 | ||
| Effect of Sea Depth on the Volume of Gases—Boyle’s Law. | 569 | ||
| Effect of High Partial Pressures of Individual Gases on the Body | 569 | ||
| Nitrogen Narcosis at High Nitrogen Pressures | 569 | ||
| Oxygen Toxicity at High Pressures | 569 | ||
| Effect of Very High PO2 on Blood Oxygen Transport. | 569 | ||
| Effect of High Alveolar Po2 on Tissue Po2. | 570 | ||
| Acute Oxygen Poisoning. | 570 | ||
| Excessive Intracellular Oxidation as a Cause of Nervous System Oxygen Toxicity—“Oxidizing Free Radicals.” | 570 | ||
| Chronic Oxygen Poisoning Causes Pulmonary Disability. | 571 | ||
| Carbon Dioxide Toxicity at Great Depths in the Sea | 571 | ||
| Decompression of the Diver after Excess Exposure to High Pressure | 571 | ||
| Volume of Nitrogen Dissolved in the Body Fluids at Different Depths. | 571 | ||
| Decompression Sickness (Also Known As Bends, Compressed Air Sickness, Caisson Disease, Diver’s Paralysis, Dysbarism). | 572 | ||
| Symptoms of Decompression Sickness (“Bends”). | 572 | ||
| Nitrogen Elimination from the Body; Decompression Tables. | 572 | ||
| Tank Decompression and Treatment of Decompression Sickness. | 572 | ||
| “Saturation Diving” and Use of Helium-Oxygen Mixtures in Deep Dives. | 573 | ||
| Self-Contained Underwater Breathing Apparatus (SCUBA) Diving | 573 | ||
| Special Physiological Problems in Submarines | 574 | ||
| Escape from Submarines. | 574 | ||
| Health Problems in the Submarine Internal Environment. | 574 | ||
| Hyperbaric Oxygen Therapy | 574 | ||
| Bibliography | 574 | ||
| Unit IX The Nervous System: A. General Principles and Sensory Physiology | 575 | ||
| 46 Organization of the Nervous System, Basic Functions of Synapses, and Neurotransmitters | 577 | ||
| General Design of the Nervous System | 577 | ||
| Central Nervous System Neuron: the Basic Functional Unit | 577 | ||
| Sensory Part of the Nervous System—Sensory Receptors | 577 | ||
| Motor Part of the Nervous System—Effectors | 577 | ||
| Processing of Information—“Integrative” Function of the Nervous System | 578 | ||
| Role of Synapses in Processing Information | 578 | ||
| Storage of Information—Memory | 579 | ||
| Major Levels of Central Nervous System Function | 579 | ||
| Spinal Cord Level | 579 | ||
| Lower Brain or Subcortical Level | 579 | ||
| Higher Brain or Cortical Level | 580 | ||
| Comparison of the Nervous System to a Computer | 580 | ||
| Central Nervous System Synapses | 580 | ||
| Types of Synapses—Chemical and Electrical | 580 | ||
| “One-Way” Conduction at Chemical Synapses. | 581 | ||
| Physiological Anatomy of the Synapse | 581 | ||
| Presynaptic Terminals. | 582 | ||
| Mechanism by Which an Action Potential Causes Transmitter Release from the Presynaptic Terminals—Role of Calcium Ions | 582 | ||
| Action of the Transmitter Substance on the Postsynaptic Neuron—Function of “Receptor Proteins” | 582 | ||
| Ion Channels. | 583 | ||
| “Second Messenger” System in the Postsynaptic Neuron. | 583 | ||
| Excitatory or Inhibitory Receptors in the Postsynaptic Membrane | 584 | ||
| Excitation | 584 | ||
| Inhibition | 584 | ||
| Chemical Substances That Function as Synaptic Transmitters | 584 | ||
| Small-Molecule, Rapidly Acting Transmitters | 585 | ||
| Recycling of the Small-Molecule Types of Vesicles. | 585 | ||
| Characteristics of Some Important Small-Molecule Transmitters. | 586 | ||
| Neuropeptides | 586 | ||
| Electrical Events during Neuronal Excitation | 587 | ||
| Resting Membrane Potential of the Neuronal Soma. | 587 | ||
| Concentration Differences of Ions Across the Neuronal Somal Membrane. | 587 | ||
| Uniform Distribution of Electrical Potential Inside the Soma. | 588 | ||
| Effect of Synaptic Excitation on the Postsynaptic Membrane—Excitatory Postsynaptic Potential. | 588 | ||
| Generation of Action Potentials in the Initial Segment of the Axon Leaving the Neuron—Threshold for Excitation. | 588 | ||
| Electrical Events during Neuronal Inhibition | 589 | ||
| Effect of Inhibitory Synapses on the Postsynaptic Membrane—Inhibitory Postsynaptic Potential. | 589 | ||
| Presynaptic Inhibition | 589 | ||
| Time Course of Postsynaptic Potentials | 589 | ||
| “Spatial Summation” in Neurons—Threshold for Firing | 590 | ||
| “Temporal Summation” Caused by Successive Discharges of a Presynaptic Terminal | 590 | ||
| Simultaneous Summation of Inhibitory and Excitatory Postsynaptic Potentials. | 590 | ||
| “Facilitation” of Neurons | 590 | ||
| Special Functions of Dendrites for Exciting Neurons | 590 | ||
| Large Spatial Field of Excitation of the Dendrites. | 590 | ||
| Most Dendrites Cannot Transmit Action Potentials, but They Can Transmit Signals Within the Same Neuron by Electrotonic Conduction. | 590 | ||
| Decrement of Electrotonic Conduction in the Dendrites—Greater Excitatory (or Inhibitory) Effect by Synapses Located Near the Soma. | 591 | ||
| Summation of Excitation and Inhibition in Dendrites. | 591 | ||
| Relation of State of Excitation of the Neuron to Rate of Firing | 591 | ||
| “Excitatory State” Is the Summated Degree of Excitatory Drive to the Neuron. | 591 | ||
| Some Special Characteristics of Synaptic Transmission | 592 | ||
| Fatigue of Synaptic Transmission. | 592 | ||
| Effect of Acidosis or Alkalosis on Synaptic Transmission. | 592 | ||
| Effect of Hypoxia on Synaptic Transmission. | 592 | ||
| Effect of Drugs on Synaptic Transmission. | 592 | ||
| Synaptic Delay. | 592 | ||
| Bibliography | 593 | ||
| 47 Sensory Receptors, Neuronal Circuits for Processing Information | 595 | ||
| Types of Sensory Receptors and the Stimuli They Detect | 595 | ||
| Differential Sensitivity of Receptors | 595 | ||
| Modality of Sensation—The “Labeled Line” Principle | 595 | ||
| Transduction of Sensory Stimuli Into Nerve Impulses | 596 | ||
| Local Electrical Currents at Nerve Endings—Receptor Potentials | 596 | ||
| Mechanisms of Receptor Potentials. | 596 | ||
| Maximum Receptor Potential Amplitude. | 597 | ||
| Relation of the Receptor Potential to Action Potentials. | 597 | ||
| Receptor Potential of the Pacinian Corpuscle—an Example of Receptor Function | 597 | ||
| Relation between Stimulus Intensity and the Receptor Potential. | 597 | ||
| Adaptation of Receptors | 598 | ||
| Mechanisms by Which Receptors Adapt. | 598 | ||
| Slowly Adapting Receptors Detect Continuous Stimulus Strength—the “Tonic” Receptors. | 598 | ||
| Rapidly Adapting Receptors Detect Change in Stimulus Strength—the “Rate Receptors,” “Movement Receptors,” or “Phasic Receptors.” | 599 | ||
| Predictive Function of the Rate Receptors. | 599 | ||
| Nerve Fibers That Transmit Different Types of Signals and Their Physiological Classification | 599 | ||
| General Classification of Nerve Fibers. | 599 | ||
| Alternative Classification Used by Sensory Physiologists. | 600 | ||
| Group Ia. | 600 | ||
| Group Ib. | 600 | ||
| Group II. | 600 | ||
| Group III. | 600 | ||
| Group IV. | 600 | ||
| Transmission of Signals of Different Intensity in Nerve Tracts—Spatial and Temporal Summation | 600 | ||
| Spatial Summation. | 600 | ||
| Temporal Summation. | 600 | ||
| Transmission and Processing of Signals in Neuronal Pools | 601 | ||
| Relaying of Signals Through Neuronal Pools | 601 | ||
| Organization of Neurons for Relaying Signals. | 601 | ||
| Threshold and Subthreshold Stimuli—Excitation or Facilitation. | 601 | ||
| Inhibition of a Neuronal Pool. | 602 | ||
| Divergence of Signals Passing Through Neuronal Pools | 602 | ||
| Convergence of Signals | 602 | ||
| Neuronal Circuit With Both Excitatory and Inhibitory Output Signals | 603 | ||
| Prolongation of a Signal by a Neuronal Pool—“Afterdischarge” | 603 | ||
| Synaptic Afterdischarge. | 603 | ||
| Reverberatory (Oscillatory) Circuit as a Cause of Signal Prolongation. | 603 | ||
| Characteristics of Signal Prolongation From a Reverberatory Circuit. | 604 | ||
| Continuous Signal Output from Some Neuronal Circuits | 604 | ||
| Continuous Discharge Caused by Intrinsic Neuronal Excitability. | 604 | ||
| Continuous Signals Emitted from Reverberating Circuits as a Means for Transmitting Information. | 604 | ||
| Rhythmical Signal Output | 604 | ||
| Instability and Stability of Neuronal Circuits | 605 | ||
| Inhibitory Circuits as a Mechanism for Stabilizing Nervous System Function | 605 | ||
| Synaptic Fatigue as a Means of Stabilizing the Nervous System | 605 | ||
| Automatic Short-Term Adjustment of Pathway Sensitivity by the Fatigue Mechanism. | 605 | ||
| Long-Term Changes in Synaptic Sensitivity Caused by Automatic Down-Regulation or Up-Regulation of Synaptic Receptors. | 606 | ||
| Bibliography | 606 | ||
| 48 Somatic Sensations: | 607 | ||
| Classification of Somatic Senses | 607 | ||
| Other Classifications of Somatic Sensations. | 607 | ||
| Detection and Transmission of Tactile Sensations | 607 | ||
| Interrelations Among the Tactile Sensations of Touch, Pressure, and Vibration. | 607 | ||
| Tactile Receptors. | 607 | ||
| Transmission of Tactile Signals in Peripheral Nerve Fibers. | 608 | ||
| Detection of Vibration. | 608 | ||
| Detection of Tickle and Itch by Mechanoreceptive Free Nerve Endings. | 608 | ||
| Sensory Pathways for Transmitting Somatic Signals Into the Central Nervous System | 609 | ||
| Dorsal Column–Medial Lemniscal System | 609 | ||
| Anterolateral System | 609 | ||
| Transmission in the Dorsal Column–Medial Lemniscal System | 609 | ||
| Anatomy of the Dorsal Column–Medial Lemniscal System | 609 | ||
| Dorsal Column–Medial Lemniscal Pathway. | 610 | ||
| Spatial Orientation of the Nerve Fibers in the Dorsal Column–Medial Lemniscal System | 610 | ||
| Somatosensory Cortex | 611 | ||
| Somatosensory Areas I and II. | 611 | ||
| Spatial Orientation of Signals from Different Parts of the Body in Somatosensory Area I. | 612 | ||
| Layers of the Somatosensory Cortex and Their Function | 612 | ||
| The Sensory Cortex Is Organized in Vertical Columns of Neurons; Each Column Detects a Different Sensory Spot on the Body with a Specific Sensory Modality | 613 | ||
| Functions of Somatosensory Area I | 613 | ||
| Somatosensory Association Areas | 613 | ||
| Effect of Removing the Somatosensory Association Area—Amorphosynthesis. | 613 | ||
| Overall Characteristics of Signal Transmission and Analysis in the Dorsal Column–Medial Lemniscal System | 614 | ||
| Basic Neuronal Circuit in the Dorsal Column–Medial Lemniscal System. | 614 | ||
| Two-Point Discrimination. | 614 | ||
| Effect of Lateral Inhibition (Also Called Surround Inhibition) to Increase the Degree of Contrast in the Perceived Spatial Pattern. | 615 | ||
| Transmission of Rapidly Changing and Repetitive Sensations. | 615 | ||
| Vibratory Sensation. | 615 | ||
| Interpretation of Sensory Stimulus Intensity | 615 | ||
| Importance of the Tremendous Intensity Range of Sensory Reception. | 615 | ||
| Judgment of Stimulus Intensity | 615 | ||
| Weber-Fechner Principle—Detection of “Ratio” of Stimulus Strength. | 615 | ||
| Power Law. | 616 | ||
| Position Senses | 616 | ||
| Position Sensory Receptors. | 616 | ||
| Processing of Position Sense Information in the Dorsal Column–Medial Lemniscal Pathway. | 616 | ||
| Transmission of Less Critical Sensory Signals in the Anterolateral Pathway | 616 | ||
| Anatomy of the Anterolateral Pathway | 617 | ||
| Characteristics of Transmission in the Anterolateral Pathway | 617 | ||
| Some Special Aspects of Somatosensory Function | 618 | ||
| Function of the Thalamus in Somatic Sensation | 618 | ||
| Cortical Control of Sensory Sensitivity—“Corticofugal” Signals | 618 | ||
| Segmental Fields of Sensation—Dermatomes | 618 | ||
| Bibliography | 618 | ||
| 49 Somatic Sensations: | 621 | ||
| Types of Pain and Their Qualities—Fast Pain and Slow Pain | 621 | ||
| Pain Receptors and Their Stimulation | 621 | ||
| Pain Receptors Are Free Nerve Endings. | 621 | ||
| Three Types of Stimuli Excite Pain Receptors—Mechanical, Thermal, and Chemical. | 621 | ||
| Nonadapting Nature of Pain Receptors. | 621 | ||
| Rate of Tissue Damage as a Stimulus for Pain | 622 | ||
| Special Importance of Chemical Pain Stimuli During Tissue Damage. | 622 | ||
| Tissue Ischemia as a Cause of Pain. | 622 | ||
| Muscle Spasm as a Cause of Pain. | 622 | ||
| Dual Pathways for Transmission of Pain Signals Into the Central Nervous System | 622 | ||
| Peripheral Pain Fibers—“Fast” and “Slow” Fibers | 622 | ||
| Dual Pain Pathways in the Cord and Brain Stem—the Neospinothalamic Tract and the Paleospinothalamic Tract | 623 | ||
| Neospinothalamic Tract for Fast Pain. | 623 | ||
| Termination of the Neospinothalamic Tract in the Brain Stem and Thalamus. | 623 | ||
| Capability of the Nervous System to Localize Fast Pain in the Body. | 623 | ||
| Glutamate, the Probable Neurotransmitter of the Type Aδ Fast Pain Fibers. | 623 | ||
| Paleospinothalamic Pathway for Transmitting Slow-Chronic Pain. | 623 | ||
| Substance P, the Probable Slow-Chronic Neurotransmitter of Type C Nerve Endings. | 624 | ||
| Projection of the Paleospinothalamic Pathway (Slow-Chronic Pain Signals) into the Brain Stem and Thalamus. | 624 | ||
| Poor Capability of the Nervous System to Localize Precisely the Source of Pain Transmitted in the Slow-Chronic Pathway. | 624 | ||
| Function of the Reticular Formation, Thalamus, and Cerebral Cortex in the Appreciation of Pain. | 624 | ||
| Special Capability of Pain Signals to Arouse Overall Brain Excitability. | 624 | ||
| Surgical Interruption of Pain Pathways. | 624 | ||
| Pain Suppression (Analgesia) System in the Brain and Spinal Cord | 625 | ||
| The Brain’s Opiate System—Endorphins and Enkephalins | 625 | ||
| Inhibition of Pain Transmission by Simultaneous Tactile Sensory Signals | 626 | ||
| Treatment of Pain by Electrical Stimulation | 626 | ||
| Referred Pain | 626 | ||
| Mechanism of Referred Pain. | 626 | ||
| Visceral Pain | 626 | ||
| Causes of True Visceral Pain | 626 | ||
| Ischemia. | 627 | ||
| Chemical Stimuli. | 627 | ||
| Spasm of a Hollow Viscus. | 627 | ||
| Overdistention of a Hollow Viscus. | 627 | ||
| Insensitive Viscera. | 627 | ||
| “Parietal Pain” Caused by Visceral Disease | 627 | ||
| Localization of Visceral Pain—“Visceral” and “Parietal” Pain Transmission Pathways | 627 | ||
| Localization of Referred Pain Transmitted via Visceral Pathways. | 627 | ||
| Parietal Pathway for Transmission of Abdominal and Thoracic Pain. | 627 | ||
| Some Clinical Abnormalities of Pain and Other Somatic Sensations | 628 | ||
| Hyperalgesia—Hypersensitivity to Pain | 628 | ||
| Herpes Zoster (Shingles) | 628 | ||
| Tic Douloureux | 628 | ||
| Brown-Séquard Syndrome | 629 | ||
| Headache | 629 | ||
| Headache of Intracranial Origin | 629 | ||
| Pain-Sensitive Areas in the Cranial Vault. | 629 | ||
| Areas of the Head to Which Intracranial Headache Is Referred. | 629 | ||
| Types of Intracranial Headache | 629 | ||
| Headache of Meningitis. | 629 | ||
| Headache Caused by Low Cerebrospinal Fluid Pressure. | 629 | ||
| Migraine Headache. | 630 | ||
| Alcoholic Headache. | 630 | ||
| Extracranial Types of Headache | 630 | ||
| Headache Resulting from Muscle Spasm. | 630 | ||
| Headache Caused by Irritation of Nasal and Accessory Nasal Structures. | 630 | ||
| Headache Caused by Eye Disorders. | 630 | ||
| Thermal Sensations | 630 | ||
| Thermal Receptors and Their Excitation | 630 | ||
| Stimulation of Thermal Receptors—Sensations of Cold, Cool, Indifferent, Warm, and Hot. | 631 | ||
| Stimulatory Effects of Rising and Falling Temperature —Adaptation of Thermal Receptors. | 631 | ||
| Mechanism of Stimulation of Thermal Receptors | 631 | ||
| Spatial Summation of Thermal Sensations. | 631 | ||
| Transmission of Thermal Signals in the Nervous System | 631 | ||
| Bibliography | 632 | ||
| Unit X The Nervous System: B. The Special Senses | 633 | ||
| 50 The Eye: | 635 | ||
| Physical Principles of Optics | 635 | ||
| Refraction of Light | 635 | ||
| Refractive Index of a Transparent Substance. | 635 | ||
| Refraction of Light Rays at an Interface Between Two Media with Different Refractive Indices. | 635 | ||
| Application of Refractive Principles to Lenses | 635 | ||
| Convex Lens Focuses Light Rays. | 635 | ||
| Concave Lens Diverges Light Rays. | 636 | ||
| Cylindrical Lens Bends Light Rays in Only One Plane—Comparison with Spherical Lenses. | 636 | ||
| Combination of Two Cylindrical Lenses at Right Angles Equals a Spherical Lens. | 636 | ||
| Focal Length of a Lens | 636 | ||
| Formation of an Image by a Convex Lens | 637 | ||
| Measurement of the Refractive Power of a Lens—“Diopter” | 637 | ||
| Optics of the Eye | 638 | ||
| The Eye as a Camera | 638 | ||
| Consideration of All Refractive Surfaces of the Eye as a Single Lens—The “Reduced” Eye. | 638 | ||
| Formation of an Image on the Retina. | 639 | ||
| Mechanism of “Accommodation” | 639 | ||
| Accommodation Is Controlled by Parasympathetic Nerves. | 639 | ||
| Presbyopia—Loss of Accommodation by the Lens. | 640 | ||
| Pupillary Diameter | 640 | ||
| “Depth of Focus” of the Lens System Increases with Decreasing Pupillary Diameter. | 640 | ||
| Errors of Refraction | 640 | ||
| Emmetropia (Normal Vision). | 640 | ||
| Hyperopia (Farsightedness). | 641 | ||
| Myopia (Nearsightedness). | 641 | ||
| Correction of Myopia and Hyperopia Through Use of Lenses. | 641 | ||
| Astigmatism. | 641 | ||
| Correction of Astigmatism with a Cylindrical Lens. | 642 | ||
| Correction of Optical Abnormalities with Contact Lenses. | 642 | ||
| Cataracts—Opaque Areas in the Lens. | 642 | ||
| Visual Acuity | 642 | ||
| Clinical Method for Stating Visual Acuity. | 643 | ||
| Determination of Distance of an Object From the Eye—“Depth Perception” | 643 | ||
| Determination of Distance by Sizes of Retinal Images of Known Objects. | 643 | ||
| Determination of Distance by Moving Parallax. | 643 | ||
| Determination of Distance by Stereopsis—Binocular Vision. | 643 | ||
| Ophthalmoscope | 644 | ||
| Fluid System of the Eye—Intraocular Fluid | 644 | ||
| Formation of Aqueous Humor by the Ciliary Body | 644 | ||
| Outflow of Aqueous Humor From the Eye | 645 | ||
| Intraocular Pressure | 645 | ||
| Measuring Intraocular Pressure by Tonometry. | 645 | ||
| Regulation of Intraocular Pressure. | 645 | ||
| Mechanism for Cleansing the Trabecular Spaces and Intraocular Fluid. | 646 | ||
| “Glaucoma” Causes High Intraocular Pressure and Is a Principal Cause of Blindness. | 646 | ||
| Bibliography | 646 | ||
| 51 The Eye: | 647 | ||
| Anatomy and Function of the Structural Elements of the Retina | 647 | ||
| Layers of the Retina. | 647 | ||
| Foveal Region of the Retina and Its Importance in Acute Vision. | 647 | ||
| Rods and Cones. | 647 | ||
| Pigment Layer of the Retina. | 648 | ||
| Blood Supply of the Retina—The Central Retinal Artery and the Choroid. | 649 | ||
| Retinal Detachment. | 649 | ||
| Photochemistry of Vision | 649 | ||
| Rhodopsin-Retinal Visual Cycle and Excitation of the Rods | 649 | ||
| Rhodopsin and Its Decomposition by Light Energy. | 649 | ||
| Re-Formation of Rhodopsin. | 650 | ||
| Role of Vitamin A for Formation of Rhodopsin. | 650 | ||
| Night Blindness. | 650 | ||
| Excitation of the Rod When Rhodopsin Is Activated by Light | 650 | ||
| The Rod Receptor Potential is Hyperpolarizing, Not Depolarizing. | 650 | ||
| Duration of the Receptor Potential, and Logarithmic Relation of the Receptor Potential to Light Intensity. | 651 | ||
| Mechanism by Which Rhodopsin Decomposition Decreases Membrane Sodium Conductance—The Excitation “Cascade.” | 652 | ||
| Photochemistry of Color Vision by the Cones | 652 | ||
| Automatic Regulation of Retinal Sensitivity—Light and Dark Adaptation | 653 | ||
| Other Mechanisms of Light and Dark Adaptation. | 653 | ||
| Value of Light and Dark Adaptation in Vision. | 653 | ||
| Color Vision | 654 | ||
| Tricolor Mechanism of Color Detection | 654 | ||
| Spectral Sensitivities of the Three Types of Cones. | 654 | ||
| Interpretation of Color in the Nervous System. | 654 | ||
| Perception of White Light. | 654 | ||
| Color Blindness | 654 | ||
| Red-Green Color Blindness. | 654 | ||
| Blue Weakness. | 654 | ||
| Color Test Charts. | 654 | ||
| Neural Function of the Retina | 655 | ||
| The Visual Pathway from the Cones to the Ganglion Cells Functions Differently from the Rod Pathway. | 656 | ||
| Neurotransmitters Released by Retinal Neurons. | 656 | ||
| Transmission of Most Signals Occurs in the Retinal Neurons by Electrotonic Conduction, Not by Action Potentials. | 656 | ||
| Lateral Inhibition to Enhance Visual Contrast—Function of the Horizontal Cells | 656 | ||
| Depolarizing and Hyperpolarizing Bipolar Cells | 656 | ||
| Amacrine Cells and Their Functions | 657 | ||
| Ganglion Cells and Optic Nerve Fibers | 657 | ||
| Retinal Ganglion Cells and Their Respective Fields | 657 | ||
| W, X, and Y Cells. | 657 | ||
| P and M Cells. | 658 | ||
| Excitation of the Ganglion Cells | 658 | ||
| Spontaneous, Continuous Action Potentials in the Ganglion Cells. | 658 | ||
| Transmission of Changes in Light Intensity—The On-Off Response. | 658 | ||
| Transmission of Signals Depicting Contrasts in the Visual Scene—The Role of Lateral Inhibition | 659 | ||
| Transmission of Color Signals by the Ganglion Cells | 659 | ||
| Bibliography | 660 | ||
| 52 The Eye: | 661 | ||
| Visual Pathways | 661 | ||
| Function of the Dorsal Lateral Geniculate Nucleus of the Thalamus | 661 | ||
| Organization and Function of the Visual Cortex | 662 | ||
| Primary Visual Cortex. | 662 | ||
| Secondary Visual Areas of the Cortex. | 662 | ||
| The Primary Visual Cortex Has Six Major Layers | 663 | ||
| Vertical Neuronal Columns in the Visual Cortex. | 663 | ||
| “Color Blobs” in the Visual Cortex. | 663 | ||
| Interaction of Visual Signals from the Two Separate Eyes. | 663 | ||
| Two Major Pathways for Analysis of Visual Information: (1) the Fast “Position” and “Motion” Pathway and (2) the Accurate Color Pathway | 664 | ||
| Neuronal Patterns of Stimulation during Analysis of the Visual Image | 664 | ||
| Analysis of Contrasts in the Visual Image. | 664 | ||
| Visual Cortex Also Detects Orientation of Lines and Borders—“Simple” Cells. | 664 | ||
| Detection of Line Orientation When a Line Is Displaced Laterally or Vertically in the Visual Field—“Complex” Cells. | 664 | ||
| Detection of Lines of Specific Lengths, Angles, or Other Shapes. | 665 | ||
| Detection of Color | 665 | ||
| Effect of Removing the Primary Visual Cortex | 665 | ||
| Fields of Vision; Perimetry | 665 | ||
| Abnormalities in the Fields of Vision. | 665 | ||
| Effect of Lesions in the Optic Pathway on the Fields of Vision. | 665 | ||
| Eye Movements and Their Control | 666 | ||
| Muscular Control of Eye Movements. | 666 | ||
| Neural Pathways for Control of Eye Movements. | 666 | ||
| Fixation Movements of the Eyes | 667 | ||
| Mechanism of Involuntary Locking Fixation—Role of the Superior Colliculi. | 667 | ||
| Saccadic Movement of the Eyes—A Mechanism of Successive Fixation Points. | 667 | ||
| Saccadic Movements During Reading. | 667 | ||
| Fixation on Moving Objects—“Pursuit Movement.” | 668 | ||
| Superior Colliculi Are Mainly Responsible for Turning the Eyes and Head Toward a Visual Disturbance. | 668 | ||
| “Fusion” of the Visual Images from the Two Eyes | 668 | ||
| Neural Mechanism of Stereopsis for Judging Distances of Visual Objects | 668 | ||
| Strabismus—Lack of Fusion of the Eyes | 668 | ||
| Suppression of the Visual Image from a Repressed Eye. | 669 | ||
| Autonomic Control of Accommodation and Pupillary Aperture | 669 | ||
| Autonomic Nerves to the Eyes | 669 | ||
| Control of Accommodation (Focusing the Eyes) | 669 | ||
| Control of Pupillary Diameter | 670 | ||
| Pupillary Light Reflex. | 670 | ||
| Pupillary Reflexes or Reactions in Central Nervous System Disease. | 670 | ||
| Horner’s Syndrome. | 670 | ||
| Bibliography | 671 | ||
| 53 The Sense of Hearing | 673 | ||
| Tympanic Membrane and the Ossicular System | 673 | ||
| Conduction of Sound From the Tympanic Membrane to the Cochlea | 673 | ||
| “Impedance Matching” by the Ossicular System. | 673 | ||
| Attenuation of Sound by Contraction of the Tensor Tympani and Stapedius Muscles. | 674 | ||
| Transmission of Sound Through Bone | 674 | ||
| Cochlea | 674 | ||
| Functional Anatomy of the Cochlea | 674 | ||
| Basilar Membrane and Resonance in the Cochlea. | 675 | ||
| Transmission of Sound Waves in the Cochlea—“Traveling Wave” | 675 | ||
| Pattern of Vibration of the Basilar Membrane for Different Sound Frequencies. | 675 | ||
| Amplitude Pattern of Vibration of the Basilar Membrane. | 676 | ||
| Function of the Organ of Corti | 676 | ||
| Excitation of the Hair Cells. | 676 | ||
| Auditory Signals Are Transmitted Mainly by the Inner Hair Cells. | 677 | ||
| Hair Cell Receptor Potentials and Excitation of Auditory Nerve Fibers. | 677 | ||
| Endocochlear Potential. | 677 | ||
| Determination of Sound Frequency—the “Place” Principle | 677 | ||
| Determination of Loudness | 678 | ||
| Detection of Changes in Loudness—The Power Law. | 678 | ||
| Decibel Unit. | 678 | ||
| Threshold for Hearing Sound at Different Frequencies. | 678 | ||
| Frequency Range of Hearing. | 679 | ||
| Central Auditory Mechanisms | 679 | ||
| Auditory Nervous Pathways | 679 | ||
| Firing Rates at Different Levels of the Auditory Pathways. | 679 | ||
| Function of the Cerebral Cortex in Hearing | 680 | ||
| Sound Frequency Perception in the Primary Auditory Cortex. | 680 | ||
| Discrimination of Sound “Patterns” by the Auditory Cortex. | 681 | ||
| Determination of the Direction From Which Sound Comes | 681 | ||
| Neural Mechanisms for Detecting Sound Direction. | 681 | ||
| Centrifugal Signals From the Central Nervous System to Lower Auditory Centers | 682 | ||
| Hearing Abnormalities | 682 | ||
| Types of Deafness | 682 | ||
| Audiometer. | 682 | ||
| Audiogram in Nerve Deafness. | 682 | ||
| Audiogram for Middle Ear Conduction Deafness. | 682 | ||
| Bibliography | 683 | ||
| 54 The Chemical Senses—Taste and Smell | 685 | ||
| Sense of Taste | 685 | ||
| Primary Sensations of Taste | 685 | ||
| Sour Taste. | 685 | ||
| Salty Taste. | 685 | ||
| Sweet Taste. | 685 | ||
| Bitter Taste. | 685 | ||
| Umami Taste. | 686 | ||
| Threshold for Taste | 686 | ||
| Taste Blindness. | 686 | ||
| The Taste Bud and Its Function | 686 | ||
| Location of the Taste Buds. | 687 | ||
| Specificity of Taste Buds for a Primary Taste Stimulus. | 687 | ||
| Mechanism of Stimulation of Taste Buds | 687 | ||
| Receptor Potential. | 687 | ||
| Generation of Nerve Impulses by the Taste Bud. | 687 | ||
| Transmission of Taste Signals Into the Central Nervous System | 687 | ||
| Taste Reflexes Are Integrated in the Brain Stem. | 688 | ||
| Rapid Adaptation of Taste. | 688 | ||
| Taste Preference and Control of the Diet | 688 | ||
| Sense of Smell | 688 | ||
| Olfactory Membrane | 688 | ||
| Olfactory Cells Are the Receptor Cells for Smell Sensation. | 689 | ||
| Stimulation of the Olfactory Cells | 689 | ||
| Mechanism of Excitation of the Olfactory Cells. | 689 | ||
| Membrane Potentials and Action Potentials in Olfactory Cells. | 690 | ||
| Rapid Adaptation of Olfactory Sensations. | 690 | ||
| Search for the Primary Sensations of Smell | 690 | ||
| Affective Nature of Smell. | 690 | ||
| Threshold for Smell. | 690 | ||
| Gradations of Smell Intensities. | 690 | ||
| Transmission of Smell Signals Into the Central Nervous System | 691 | ||
| Transmission of Olfactory Signals into the Olfactory Bulb. | 691 | ||
| Primitive and Newer Olfactory Pathways into the Central Nervous System | 691 | ||
| The Primitive Olfactory System—The Medial Olfactory Area. | 691 | ||
| The Less Old Olfactory System—The Lateral Olfactory Area. | 691 | ||
| The Newer Pathway. | 692 | ||
| Summary. | 692 | ||
| Centrifugal Control of Activity in the Olfactory Bulb by the Central Nervous System. | 692 | ||
| Bibliography | 692 | ||
| Unit XI The Nervous System: C. Motor and Integrative Neurophysiology | 693 | ||
| 55 Motor Functions of the Spinal Cord; the Cord Reflexes | 695 | ||
| Organization of the Spinal Cord for Motor Functions | 695 | ||
| Anterior Motor Neurons. | 695 | ||
| Alpha Motor Neurons. | 695 | ||
| Gamma Motor Neurons. | 696 | ||
| Interneurons. | 696 | ||
| Renshaw Cells Transmit Inhibitory Signals to Surrounding Motor Neurons. | 696 | ||
| Multisegmental Connections from One Spinal Cord Level to Other Levels—Propriospinal Fibers. | 696 | ||
| Muscle Sensory Receptors—Muscle Spindles and Golgi Tendon Organs—and Their Roles in Muscle Control | 697 | ||
| Receptor Function of the Muscle Spindle | 697 | ||
| Structure and Motor Innervation of the Muscle Spindle. | 697 | ||
| Sensory Innervation of the Muscle Spindle. | 697 | ||
| Primary Ending. | 697 | ||
| Secondary Ending. | 697 | ||
| Division of the Intrafusal Fibers Into Nuclear Bag and Nuclear Chain Fibers—Dynamic and Static Responses of the Muscle Spindle. | 698 | ||
| Response of Both the Primary and the Secondary Endings to the Length of the Receptor—“Static” Response. | 698 | ||
| Response of the Primary Ending (but Not the Secondary Ending) to Rate of Change of Receptor Length—“Dynamic” Response. | 698 | ||
| Control of Intensity of the Static and Dynamic Responses by the Gamma Motor Nerves. | 698 | ||
| Continuous Discharge of the Muscle Spindles Under Normal Conditions. | 698 | ||
| Muscle Stretch Reflex | 698 | ||
| Neuronal Circuitry of the Stretch Reflex. | 698 | ||
| Dynamic Stretch Reflex and Static Stretch Reflexes. | 698 | ||
| “Damping” Function of the Dynamic and Static Stretch Reflexes in Smoothing Muscle Contraction. | 699 | ||
| Role of the Muscle Spindle in Voluntary Motor Activity | 699 | ||
| Brain Areas for Control of the Gamma Motor System | 700 | ||
| The Muscle Spindle System Stabilizes Body Position During Tense Action. | 700 | ||
| Clinical Applications of the Stretch Reflex | 700 | ||
| Knee Jerk and Other Muscle Jerks Can Be Used to Assess Sensitivity of Stretch Reflexes. | 700 | ||
| Clonus—Oscillation of Muscle Jerks. | 700 | ||
| Golgi Tendon Reflex | 701 | ||
| Golgi Tendon Organ Helps Control Muscle Tension. | 701 | ||
| Transmission of Impulses from the Tendon Organ Into the Central Nervous System. | 701 | ||
| The Tendon Reflex Prevents Excessive Tension on the Muscle. | 701 | ||
| Possible Role of the Tendon Reflex to Equalize Contractile Force Among the Muscle Fibers. | 701 | ||
| Function of the Muscle Spindles and Golgi Tendon Organs in Motor Control by Higher Levels of the Brain | 702 | ||
| Flexor Reflex and the Withdrawal Reflexes | 702 | ||
| Neuronal Mechanism of the Flexor Reflex. | 702 | ||
| Pattern of Withdrawal During Flexor Reflex. | 703 | ||
| Crossed Extensor Reflex | 703 | ||
| Neuronal Mechanism of the Crossed Extensor Reflex. | 703 | ||
| Reciprocal Inhibition and Reciprocal Innervation | 703 | ||
| Reflexes of Posture and Locomotion | 704 | ||
| Postural and Locomotive Reflexes of the Cord | 704 | ||
| Positive Supportive Reaction. | 704 | ||
| Cord “Righting” Reflexes. | 704 | ||
| Stepping and Walking Movements | 704 | ||
| Rhythmical Stepping Movements of a Single Limb. | 704 | ||
| Reciprocal Stepping of Opposite Limbs. | 704 | ||
| Diagonal Stepping of All Four Limbs—“Mark Time” Reflex. | 704 | ||
| Galloping Reflex. | 704 | ||
| Scratch Reflex | 705 | ||
| Spinal Cord Reflexes That Cause Muscle Spasm | 705 | ||
| Muscle Spasm Resulting From a Broken Bone. | 705 | ||
| Abdominal Muscle Spasm in Persons with Peritonitis. | 705 | ||
| Muscle Cramps. | 705 | ||
| Autonomic Reflexes in the Spinal Cord | 705 | ||
| Mass Reflex. | 705 | ||
| Spinal Cord Transection and Spinal Shock | 705 | ||
| Bibliography | 706 | ||
| 56 Cortical and Brain Stem Control of Motor Function | 707 | ||
| Motor Cortex and Corticospinal Tract | 707 | ||
| Primary Motor Cortex | 707 | ||
| Premotor Area | 708 | ||
| Supplementary Motor Area | 708 | ||
| Some Specialized Areas of Motor Control Found in the Human Motor Cortex | 708 | ||
| Broca’s Area (Motor Speech Area). | 709 | ||
| “Voluntary” Eye Movement Field. | 709 | ||
| Head Rotation Area. | 709 | ||
| Area for Hand Skills. | 709 | ||
| Transmission of Signals From the Motor Cortex to the Muscles | 709 | ||
| Corticospinal (Pyramidal) Tract | 709 | ||
| Other Fiber Pathways From the Motor Cortex. | 710 | ||
| Incoming Sensory Fiber Pathways to the Motor Cortex | 710 | ||
| The Red Nucleus Serves as an Alternative Pathway for Transmitting Cortical Signals to the Spinal Cord | 710 | ||
| Function of the Corticorubrospinal System. | 711 | ||
| “Extrapyramidal” System | 711 | ||
| Excitation of the Spinal Cord Motor Control Areas by the Primary Motor Cortex and Red Nucleus | 711 | ||
| Vertical Columnar Arrangement of the Neurons in the Motor Cortex. | 711 | ||
| Function of Each Column of Neurons. | 711 | ||
| Dynamic and Static Signals Are Transmitted by the Pyramidal Neurons. | 711 | ||
| Somatosensory Feedback to the Motor Cortex Helps Control the Precision of Muscle Contraction | 712 | ||
| Stimulation of the Spinal Motor Neurons | 712 | ||
| Patterns of Movement Elicited by Spinal Cord Centers. | 712 | ||
| Effect of Lesions in the Motor Cortex or in the Corticospinal Pathway—The “Stroke” | 713 | ||
| Removal of the Primary Motor Cortex (Area Pyramidalis). | 713 | ||
| Muscle Spasticity Caused by Lesions That Damage Large Areas Adjacent to the Motor Cortex. | 713 | ||
| Control of Motor Functions by the Brain Stem | 713 | ||
| Support of the Body Against Gravity—Roles of the Reticular and Vestibular Nuclei | 713 | ||
| Excitatory-Inhibitory Antagonism Between Pontine and Medullary Reticular Nuclei | 713 | ||
| Pontine Reticular System. | 714 | ||
| Medullary Reticular System. | 714 | ||
| Role of the Vestibular Nuclei to Excite the Antigravity Muscles | 714 | ||
| The Decerebrate Animal Develops Spastic Rigidity. | 714 | ||
| Vestibular Sensations and Maintenance of Equilibrium | 714 | ||
| Vestibular Apparatus | 714 | ||
| “Maculae”—Sensory Organs of the Utricle and Saccule for Detecting Orientation of the Head With Respect to Gravity. | 715 | ||
| Directional Sensitivity of the Hair Cells—Kinocilium. | 715 | ||
| Semicircular Ducts. | 716 | ||
| Function of the Utricle and Saccule in the Maintenance of Static Equilibrium | 716 | ||
| Detection of Linear Acceleration by the Utricle and Saccule Maculae. | 717 | ||
| Detection of Head Rotation by the Semicircular Ducts | 717 | ||
| “Predictive” Function of the Semicircular Duct System in the Maintenance of Equilibrium. | 717 | ||
| Vestibular Mechanisms for Stabilizing the Eyes | 718 | ||
| Other Factors Concerned With Equilibrium | 718 | ||
| Neck Proprioceptors. | 718 | ||
| Proprioceptive and Exteroceptive Information From Other Parts of the Body. | 718 | ||
| Importance of Visual Information in the Maintenance of Equilibrium. | 718 | ||
| Neuronal Connections of the Vestibular Apparatus With the Central Nervous System | 718 | ||
| Functions of Brain Stem Nuclei in Controlling Subconscious, Stereotyped Movements | 719 | ||
| Bibliography | 719 | ||
| 57 Contributions of the Cerebellum and Basal Ganglia to Overall Motor Control | 721 | ||
| The Cerebellum and Its Motor Functions | 721 | ||
| Anatomical and Functional Areas of the Cerebellum | 721 | ||
| Longitudinal Functional Divisions of the Anterior and Posterior Lobes. | 721 | ||
| Topographical Representation of the Body in the Vermis and Intermediate Zones. | 722 | ||
| Neuronal Circuit of the Cerebellum | 722 | ||
| Input Pathways to the Cerebellum | 722 | ||
| Afferent Pathways From Other Parts of the Brain. | 722 | ||
| Afferent Pathways From the Periphery. | 723 | ||
| Output Signals From the Cerebellum | 723 | ||
| Deep Cerebellar Nuclei and the Efferent Pathways. | 723 | ||
| Functional Unit of the Cerebellar Cortex—The Purkinje and Deep Nuclear Cells | 724 | ||
| Neuronal Circuit of the Functional Unit. | 724 | ||
| Purkinje Cells and Deep Nuclear Cells Fire Continuously Under Normal Resting Conditions. | 725 | ||
| Balance Between Excitation and Inhibition at the Deep Cerebellar Nuclei. | 725 | ||
| Other Inhibitory Cells in the Cerebellum. | 725 | ||
| Turn-On/Turn-Off and Turn-Off/Turn-On Output Signals from the Cerebellum | 725 | ||
| The Purkinje Cells “Learn” to Correct Motor Errors—Role of the Climbing Fibers | 726 | ||
| Function of the Cerebellum in Overall Motor Control | 726 | ||
| The Vestibulocerebellum Functions in Association With the Brain Stem and Spinal Cord to Control Equilibrium and Postural Movements | 727 | ||
| Spinocerebellum—Feedback Control of Distal Limb Movements by Way of the Intermediate Cerebellar Cortex and the Interposed Nucleus | 727 | ||
| Function of the Cerebellum to Prevent Overshoot and to “Damp” Movements. | 728 | ||
| Cerebellar Control of Ballistic Movements. | 728 | ||
| Cerebrocerebellum—Function of the Large Lateral Zone of the Cerebellar Hemisphere to Plan, Sequence, and Time Complex Movements | 728 | ||
| Planning of Sequential Movements. | 729 | ||
| Timing Function for Sequential Movements. | 729 | ||
| Extramotor Predictive Functions of the Cerebrocerebellum. | 729 | ||
| Clinical Abnormalities of the Cerebellum | 729 | ||
| Dysmetria and Ataxia | 729 | ||
| Past Pointing | 729 | ||
| Failure of Progression | 730 | ||
| Dysdiadochokinesia—Inability to Perform Rapid Alternating Movements. | 730 | ||
| Dysarthria—Failure of Progression in Talking. | 730 | ||
| Intention Tremor. | 730 | ||
| Cerebellar Nystagmus—Tremor of the Eyeballs. | 730 | ||
| Hypotonia—Decreased Tone of the Musculature | 730 | ||
| The Basal Ganglia and Their Motor Functions | 730 | ||
| Neuronal Circuitry of the Basal Ganglia | 731 | ||
| Function of the Basal Ganglia in Executing Patterns of Motor Activity—the Putamen Circuit | 731 | ||
| Neural Pathways of the Putamen Circuit. | 731 | ||
| Abnormal Function in the Putamen Circuit: Athetosis, Hemiballismus, and Chorea. | 732 | ||
| Role of the Basal Ganglia for Cognitive Control of Sequences of Motor Patterns—the Caudate Circuit | 732 | ||
| Function of the Basal Ganglia to Change the Timing and to Scale the Intensity of Movements | 732 | ||
| Functions of Specific Neurotransmitter Substances in the Basal Ganglial System | 733 | ||
| Clinical Syndromes Resulting From Damage to the Basal Ganglia | 734 | ||
| Parkinson’s Disease | 734 | ||
| Treatment With l-Dopa. | 734 | ||
| Treatment With l-Deprenyl. | 734 | ||
| Treatment With Transplanted Fetal Dopamine Cells. | 734 | ||
| Treatment by Destroying Part of the Feedback Circuitry in the Basal Ganglia. | 734 | ||
| Huntington’s Disease (Huntington’s Chorea) | 734 | ||
| Integration of the Many Parts of the Total Motor Control System | 735 | ||
| Spinal Level | 735 | ||
| Hindbrain Level | 735 | ||
| Motor Cortex Level | 735 | ||
| Associated Functions of the Cerebellum. | 735 | ||
| Associated Functions of the Basal Ganglia. | 735 | ||
| What Drives Us to Action? | 736 | ||
| Bibliography | 736 | ||
| 58 Cerebral Cortex, Intellectual Functions of the Brain, Learning, and Memory | 737 | ||
| Physiological Anatomy of the Cerebral Cortex | 737 | ||
| Anatomical and Functional Relations of the Cerebral Cortex to the Thalamus and Other Lower Centers | 738 | ||
| Functions of Specific Cortical Areas | 738 | ||
| Association Areas | 739 | ||
| Parieto-occipitotemporal Association Area | 739 | ||
| Analysis of the Spatial Coordinates of the Body. | 739 | ||
| Wernicke’s Area Is Important for Language Comprehension. | 740 | ||
| The Angular Gyrus Area Is Needed for Initial Processing of Visual Language (Reading). | 740 | ||
| Area for Naming Objects. | 740 | ||
| Prefrontal Association Area | 740 | ||
| Broca’s Area Provides the Neural Circuitry for Word Formation. | 740 | ||
| Limbic Association Area | 740 | ||
| Area for Recognition of Faces | 740 | ||
| Comprehensive Interpretative Function of the Posterior Superior Temporal Lobe—“Wernicke’s Area” (a General Interpretative Area) | 741 | ||
| Angular Gyrus—Interpretation of Visual Information. | 741 | ||
| Concept of the Dominant Hemisphere | 741 | ||
| Role of Language in the Function of Wernicke’s Area and in Intellectual Functions | 742 | ||
| Functions of the Parieto-Occipitotemporal Cortex in the Nondominant Hemisphere | 742 | ||
| Higher Intellectual Functions of the Prefrontal Association Areas | 742 | ||
| Decreased Aggressiveness and Inappropriate Social Responses. | 743 | ||
| Inability to Progress Toward Goals or to Carry Through Sequential Thoughts. | 743 | ||
| Elaboration of Thought, Prognostication, and Performance of Higher Intellectual Functions by the Prefrontal Areas—Concept of a “Working Memory.” | 743 | ||
| Function of the Brain in Communication—Language Input and Language Output | 743 | ||
| Sensory Aspects of Communication | 744 | ||
| Wernicke’s Aphasia and Global Aphasia. | 744 | ||
| Motor Aspects of Communication | 744 | ||
| Loss of Broca’s Area Causes Motor Aphasia. | 744 | ||
| Articulation. | 744 | ||
| Summary | 744 | ||
| Function of the Corpus Callosum and Anterior Commissure to Transfer Thoughts, Memories, Training, and Other Information between the Two Cerebral Hemispheres | 745 | ||
| Thoughts, Consciousness, and Memory | 745 | ||
| Memory—Roles of Synaptic Facilitation and Synaptic Inhibition | 746 | ||
| Positive and Negative Memory—“Sensitization” or “Habituation” of Synaptic Transmission. | 746 | ||
| Classification of Memories. | 746 | ||
| Short-Term Memory | 746 | ||
| Intermediate Long-Term Memory | 747 | ||
| Memory Based on Chemical Changes in Presynaptic Terminals or Postsynaptic Neuronal Membranes | 747 | ||
| Molecular Mechanism of Intermediate Memory | 747 | ||
| Mechanism for Habituation. | 747 | ||
| Mechanism for Facilitation. | 747 | ||
| Long-Term Memory | 748 | ||
| Structural Changes Occur in Synapses During Development of Long-Term Memory | 748 | ||
| Number of Neurons and Their Connectivities Often Change Significantly During Learning | 748 | ||
| Consolidation of Memory | 748 | ||
| Rehearsal Enhances the Transference of Short-Term Memory Into Long-Term Memory. | 749 | ||
| New Memories Are Codified During Consolidation. | 749 | ||
| Role of Specific Parts of the Brain in the Memory Process | 749 | ||
| The Hippocampus Promotes Storage of Memories—Anterograde Amnesia Occurs After Hippocampal Lesions Are Sustained. | 749 | ||
| Retrograde Amnesia—Inability to Recall Memories From the Past. | 749 | ||
| Hippocampi Are Not Important in Reflexive Learning. | 749 | ||
| Bibliography | 749 | ||
| 59 Behavioral and Motivational Mechanisms of the Brain—The Limbic System and the Hypothalamus | 751 | ||
| Activating—Driving Systems of the Brain | 751 | ||
| Control of Cerebral Activity by Continuous Excitatory Signals From the Brain Stem | 751 | ||
| Reticular Excitatory Area of the Brain Stem | 751 | ||
| Excitation of the Excitatory Area by Peripheral Sensory Signals. | 751 | ||
| Increased Activity of the Excitatory Area Caused by Feedback Signals Returning From the Cerebral Cortex. | 752 | ||
| The Thalamus Is a Distribution Center That Controls Activity in Specific Regions of the Cortex. | 752 | ||
| A Reticular Inhibitory Area Is Located in the Lower Brain Stem | 752 | ||
| Neurohormonal Control of Brain Activity | 752 | ||
| Neurohormonal Systems in the Human Brain. | 752 | ||
| Other Neurotransmitters and Neurohormonal Substances Secreted in the Brain. | 754 | ||
| Limbic System | 754 | ||
| Functional Anatomy of the Limbic System; Key Position of the Hypothalamus | 754 | ||
| The Hypothalamus, a Major Control Headquarters for the Limbic System | 755 | ||
| Vegetative and Endocrine Control Functions of the Hypothalamus | 755 | ||
| Cardiovascular Regulation. | 755 | ||
| Body Temperature Regulation. | 756 | ||
| Body Water Regulation. | 756 | ||
| Regulation of Uterine Contractility and Milk Ejection from the Breasts. | 756 | ||
| Gastrointestinal and Feeding Regulation. | 757 | ||
| Hypothalamic Control of Endocrine Hormone Secretion by the Anterior Pituitary Gland. | 757 | ||
| Summary. | 757 | ||
| Behavioral Functions of the Hypothalamus and Associated Limbic Structures | 757 | ||
| Effects Caused by Stimulation of the Hypothalamus. | 757 | ||
| Effects Caused by Hypothalamic Lesions. | 757 | ||
| “Reward” and “Punishment” Function of the Limbic System | 757 | ||
| Reward Centers | 758 | ||
| Punishment Centers | 758 | ||
| Association of Rage With Punishment Centers | 758 | ||
| Placidity and Tameness. | 758 | ||
| Importance of Reward or Punishment on Behavior | 758 | ||
| Effect of Tranquilizers on the Reward or Punishment Centers. | 758 | ||
| Importance of Reward or Punishment in Learning and Memory—Habituation Versus Reinforcement | 758 | ||
| Specific Functions of Other Parts of the Limbic System | 759 | ||
| Functions of the Hippocampus | 759 | ||
| Role of the Hippocampus in Learning | 759 | ||
| Anterograde Amnesia After Bilateral Removal of the Hippocampi. | 759 | ||
| Theoretical Function of the Hippocampus in Learning. | 759 | ||
| Functions of the Amygdala | 760 | ||
| Effects of Stimulating the Amygdala. | 760 | ||
| Effects of Bilateral Ablation of the Amygdala—The Klüver-Bucy Syndrome. | 760 | ||
| Overall Function of the Amygdalas. | 760 | ||
| Function of the Limbic Cortex | 760 | ||
| Ablation of the Anterior Temporal Cortex. | 760 | ||
| Ablation of the Posterior Orbital Frontal Cortex. | 760 | ||
| Ablation of the Anterior Cingulate Gyri and Subcallosal Gyri. | 760 | ||
| Summary. | 761 | ||
| Bibliography | 761 | ||
| 60 States of Brain Activity—Sleep, Brain Waves, Epilepsy, Psychoses, and Dementia | 763 | ||
| Sleep | 763 | ||
| Two Types of Sleep—Slow-Wave Sleep and Rapid Eye Movement Sleep | 763 | ||
| REM (Paradoxical, Desynchronized) Sleep | 763 | ||
| Slow-Wave Sleep | 763 | ||
| Basic Theories of Sleep | 764 | ||
| Sleep Is Caused by an Active Inhibitory Process. | 764 | ||
| Neuronal Centers, Neurohumoral Substances, and Mechanisms That Can Cause Sleep—A Possible Specific Role for Serotonin | 764 | ||
| Lesions in Sleep-Promoting Centers Can Cause Intense Wakefulness. | 765 | ||
| Other Possible Transmitter Substances Related to Sleep. | 765 | ||
| Possible Cause of REM Sleep. | 765 | ||
| Cycle Between Sleep and Wakefulness | 765 | ||
| Orexin Neurons Are Important in Arousal and Wakefulness. | 765 | ||
| Sleep Has Important Physiological Functions | 765 | ||
| Brain Waves | 766 | ||
| Origin of Brain Waves | 767 | ||
| Origin of Alpha Waves. | 767 | ||
| Origin of Delta Waves. | 767 | ||
| Effect of Varying Levels of Cerebral Activity on the Frequency of the EEG | 767 | ||
| Changes in the EEG at Different Stages of Wakefulness and Sleep | 767 | ||
| Seizures and Epilepsy | 768 | ||
| Focal (Partial) Epileptic Seizures | 768 | ||
| Generalized Seizures | 768 | ||
| Generalized Tonic-Clonic (Grand Mal) Seizures) | 769 | ||
| What Initiates a Generalized Tonic-Clonic Seizure? | 769 | ||
| What Stops the Generalized Tonic-Clonic Attack? | 770 | ||
| Absence Seizures (Petit Mal Seizures) | 770 | ||
| Treatment of Epilepsy | 770 | ||
| Psychotic Behavior—Roles of Specific Neurotransmitter Systems | 770 | ||
| Depression and Manic-Depressive Psychoses—Decreased Activity of the Norepinephrine and Serotonin Neurotransmitter Systems | 770 | ||
| Schizophrenia—Possible Exaggerated Function of Part of the Dopamine System | 771 | ||
| Alzheimer’s Disease—Amyloid Plaques and Depressed Memory | 771 | ||
| Alzheimer’s Disease Is Associated With Accumulation of Brain Beta-Amyloid Peptide. | 771 | ||
| Vascular Disorders May Contribute to Progression of Alzheimer’s Disease. | 772 | ||
| Bibliography | 772 | ||
| 61 The Autonomic Nervous System and the Adrenal Medulla | 773 | ||
| General Organization of the Autonomic Nervous System | 773 | ||
| Physiological Anatomy of the Sympathetic Nervous System | 773 | ||
| Preganglionic and Postganglionic Sympathetic Neurons | 773 | ||
| Sympathetic Nerve Fibers in the Skeletal Nerves. | 773 | ||
| Segmental Distribution of the Sympathetic Nerve Fibers. | 774 | ||
| Special Nature of the Sympathetic Nerve Endings in the Adrenal Medullae. | 774 | ||
| Physiological Anatomy of the Parasympathetic Nervous System | 774 | ||
| Preganglionic and Postganglionic Parasympathetic Neurons. | 775 | ||
| Basic Characteristics of Sympathetic and Parasympathetic Function | 775 | ||
| Cholinergic and Adrenergic Fibers—Secretion of Acetylcholine or Norepinephrine | 775 | ||
| Mechanisms of Transmitter Secretion and Removal at Postganglionic Endings | 776 | ||
| Secretion of Acetylcholine and Norepinephrine by Postganglionic Nerve Endings. | 776 | ||
| Synthesis of Acetylcholine, Its Destruction After Secretion, and Its Duration of Action. | 776 | ||
| Synthesis of Norepinephrine, Its Removal, and Its Duration of Action. | 776 | ||
| Receptors on the Effector Organs | 777 | ||
| Excitation or Inhibition of the Effector Cell by Changing Its Membrane Permeability. | 777 | ||
| Receptor Action by Altering Intracellular “Second Messenger” Enzymes. | 777 | ||
| Two Principal Types of Acetylcholine Receptors—Muscarinic and Nicotinic Receptors | 777 | ||
| Adrenergic Receptors—Alpha and Beta Receptors | 777 | ||
| Excitatory and Inhibitory Actions of Sympathetic and Parasympathetic Stimulation | 778 | ||
| Effects of Sympathetic and Parasympathetic Stimulation on Specific Organs | 778 | ||
| Eyes. | 778 | ||
| Glands of the Body. | 778 | ||
| Intramural Nerve Plexus of the Gastrointestinal System. | 780 | ||
| Heart. | 780 | ||
| Systemic Blood Vessels. | 780 | ||
| Effect of Sympathetic and Parasympathetic Stimulation on Arterial Pressure. | 780 | ||
| Effects of Sympathetic and Parasympathetic Stimulation on Other Functions of the Body. | 780 | ||
| Function of the Adrenal Medullae | 780 | ||
| Value of the Adrenal Medullae to the Function of the Sympathetic Nervous System. | 781 | ||
| Relation of Stimulus Rate to Degree of Sympathetic and Parasympathetic Effect | 781 | ||
| Sympathetic and Parasympathetic “Tone” | 781 | ||
| Tone Caused by Basal Secretion of Epinephrine and Norepinephrine by the Adrenal Medullae. | 781 | ||
| Effect of Loss of Sympathetic or Parasympathetic Tone After Denervation. | 781 | ||
| Denervation Supersensitivity of Sympathetic and Parasympathetic Organs After Denervation | 782 | ||
| Mechanism of Denervation Supersensitivity. | 782 | ||
| Autonomic Reflexes | 782 | ||
| Cardiovascular Autonomic Reflexes. | 782 | ||
| Gastrointestinal Autonomic Reflexes. | 782 | ||
| Other Autonomic Reflexes. | 782 | ||
| Stimulation of Discrete Organs in Some Instances and Mass Stimulation in Other Instances by the Sympathetic and Parasympathetic Systems | 783 | ||
| The Sympathetic System Sometimes Responds by Mass Discharge. | 783 | ||
| The Parasympathetic System Usually Causes Specific Localized Responses. | 783 | ||
| “Alarm” or “Stress” Response of the Sympathetic Nervous System | 783 | ||
| Medullary, Pontine, and Mesencephalic Control of the Autonomic Nervous System | 783 | ||
| Control of Brain Stem Autonomic Centers by Higher Areas. | 784 | ||
| Pharmacology of the Autonomic Nervous System | 784 | ||
| Drugs That Act on Adrenergic Effector Organs—Sympathomimetic Drugs | 784 | ||
| Drugs That Cause Release of Norepinephrine From Nerve Endings. | 784 | ||
| Drugs That Block Adrenergic Activity. | 784 | ||
| Drugs That Act on Cholinergic Effector Organs | 784 | ||
| Parasympathomimetic Drugs (Cholinergic Drugs). | 784 | ||
| Drugs That Have a Parasympathetic Potentiating Effect—Anticholinesterase Drugs. | 785 | ||
| Drugs That Block Cholinergic Activity at Effector Organs—Antimuscarinic Drugs. | 785 | ||
| Drugs That Stimulate or Block Sympathetic and Parasympathetic Postganglionic Neurons | 785 | ||
| Drugs That Stimulate Autonomic Postganglionic Neurons. | 785 | ||
| Ganglionic Blocking Drugs. | 785 | ||
| Bibliography | 785 | ||
| 62 Cerebral Blood Flow, Cerebrospinal Fluid, and Brain Metabolism | 787 | ||
| Cerebral Blood Flow | 787 | ||
| Regulation of Cerebral Blood Flow | 787 | ||
| Excesses of Carbon Dioxide or Hydrogen Ion Concentration Increase Cerebral Blood Flow. | 787 | ||
| Importance of Cerebral Blood Flow Control by Carbon Dioxide and Hydrogen Ions. | 788 | ||
| Oxygen Deficiency as a Regulator of Cerebral Blood Flow. | 788 | ||
| Substances Released from Astrocytes Regulate Cerebral Blood Flow. | 788 | ||
| Measurement of Cerebral Blood Flow and Effect of Brain Activity on Flow. | 788 | ||
| Cerebral Blood Flow Autoregulation Protects the Brain From Fluctuations in Arterial Pressure Changes. | 789 | ||
| Role of the Sympathetic Nervous System in Controlling Cerebral Blood Flow. | 789 | ||
| Cerebral Microcirculation | 789 | ||
| Cerebral “Stroke” Occurs When Cerebral Blood Vessels Are Blocked | 790 | ||
| Cerebrospinal Fluid System | 790 | ||
| Cushioning Function of the Cerebrospinal Fluid | 790 | ||
| Contrecoup. | 790 | ||
| Formation, Flow, and Absorption of Cerebrospinal Fluid | 791 | ||
| Secretion by the Choroid Plexus. | 791 | ||
| Absorption of Cerebrospinal Fluid Through the Arachnoidal Villi. | 791 | ||
| Perivascular Spaces and Cerebrospinal Fluid. | 792 | ||
| Lymphatic Function of the Perivascular Spaces. | 792 | ||
| Cerebrospinal Fluid Pressure | 792 | ||
| Regulation of Cerebrospinal Fluid Pressure by the Arachnoidal Villi. | 792 | ||
| High Cerebrospinal Fluid Pressure in Pathological Conditions of the Brain. | 792 | ||
| Measurement of Cerebrospinal Fluid Pressure. | 792 | ||
| Obstruction to Flow of Cerebrospinal Fluid Can Cause Hydrocephalus. | 793 | ||
| Blood–Cerebrospinal Fluid and Blood-Brain Barriers | 793 | ||
| Brain Edema | 793 | ||
| Brain Metabolism | 794 | ||
| Total Brain Metabolic Rate and Metabolic Rate of Neurons. | 794 | ||
| Special Requirement of the Brain for Oxygen—Lack of Significant Anaerobic Metabolism. | 794 | ||
| Under Normal Conditions, Most Brain Energy Is Supplied by Glucose. | 794 | ||
| Bibliography | 794 | ||
| Unit XII Gastrointestinal Physiology | 795 | ||
| 63 General Principles of Gastrointestinal Function—Motility, Nervous Control, and Blood Circulation | 797 | ||
| General Principles of Gastrointestinal Motility | 797 | ||
| Physiological Anatomy of the Gastrointestinal Wall | 797 | ||
| Gastrointestinal Smooth Muscle Functions as a Syncytium. | 797 | ||
| Electrical Activity of Gastrointestinal Smooth Muscle | 797 | ||
| Slow Waves. | 797 | ||
| Spike Potentials. | 798 | ||
| Changes in Voltage of the Resting Membrane Potential. | 799 | ||
| Entry of Calcium Ions Causes Smooth Muscle Contraction. | 799 | ||
| Tonic Contraction of Some Gastrointestinal Smooth Muscle. | 799 | ||
| Neural Control of Gastrointestinal Function—Enteric Nervous System | 799 | ||
| Differences between the Myenteric and Submucosal Plexuses | 800 | ||
| Types of Neurotransmitters Secreted by Enteric Neurons | 800 | ||
| Autonomic Control of the Gastrointestinal Tract | 801 | ||
| Parasympathetic Stimulation Increases Activity of the Enteric Nervous System. | 801 | ||
| Sympathetic Stimulation Usually Inhibits Gastrointestinal Tract Activity. | 801 | ||
| Afferent Sensory Nerve Fibers From the Gut | 801 | ||
| Gastrointestinal Reflexes | 801 | ||
| Hormonal Control of Gastrointestinal Motility | 802 | ||
| Functional Types of Movements in the Gastrointestinal Tract | 803 | ||
| Propulsive Movements—Peristalsis | 803 | ||
| Function of the Myenteric Plexus in Peristalsis. | 803 | ||
| Peristaltic Waves Move Toward the Anus With Downstream Receptive Relaxation—“Law of the Gut.” | 803 | ||
| Mixing Movements | 803 | ||
| Gastrointestinal Blood Flow—Splanchnic Circulation | 804 | ||
| Anatomy of the Gastrointestinal Blood Supply | 804 | ||
| Effect of Gut Activity and Metabolic Factors on Gastrointestinal Blood Flow | 804 | ||
| Possible Causes of the Increased Blood Flow During Gastrointestinal Activity. | 804 | ||
| “Countercurrent” Blood Flow in the Villi. | 805 | ||
| Nervous Control of Gastrointestinal Blood Flow | 805 | ||
| Importance of Nervous Depression of Gastrointestinal Blood Flow When Other Parts of the Body Need Extra Blood Flow. | 806 | ||
| Bibliography | 806 | ||
| 64 Propulsion and Mixing of Food in the Alimentary Tract | 807 | ||
| Ingestion of Food | 807 | ||
| Mastication (Chewing) | 807 | ||
| Swallowing (Deglutition) | 807 | ||
| Voluntary Stage of Swallowing. | 807 | ||
| Involuntary Pharyngeal Stage of Swallowing. | 808 | ||
| Nervous Initiation of the Pharyngeal Stage of Swallowing. | 808 | ||
| Effect of the Pharyngeal Stage of Swallowing on Respiration. | 808 | ||
| The Esophageal Stage of Swallowing Involves Two Types of Peristalsis. | 809 | ||
| Receptive Relaxation of the Stomach. | 809 | ||
| Function of the Lower Esophageal Sphincter (Gastroesophageal Sphincter). | 809 | ||
| Additional Prevention of Esophageal Reflux by Valvelike Closure of the Distal End of the Esophagus. | 809 | ||
| Motor Functions of the Stomach | 809 | ||
| Storage Function of the Stomach | 810 | ||
| Mixing and Propulsion of Food in the Stomach—Basic Electrical Rhythm of the Stomach Wall | 810 | ||
| Chyme. | 810 | ||
| Hunger Contractions. | 810 | ||
| Stomach Emptying | 811 | ||
| Intense Antral Peristaltic Contractions During Stomach Emptying—“Pyloric Pump.” | 811 | ||
| Role of the Pylorus in Controlling Stomach Emptying. | 811 | ||
| Regulation of Stomach Emptying | 811 | ||
| Gastric Factors That Promote Emptying | 811 | ||
| Effect of Gastric Food Volume on Rate of Emptying. | 811 | ||
| Effect of the Hormone Gastrin on Stomach Emptying. | 811 | ||
| Powerful Duodenal Factors That Inhibit Stomach Emptying | 811 | ||
| Inhibitory Effect of Enterogastric Nervous Reflexes From the Duodenum. | 811 | ||
| Hormonal Feedback From the Duodenum Inhibits Gastric Emptying—Role of Fats and the Hormone Cholecystokinin. | 812 | ||
| Summary of the Control of Stomach Emptying | 812 | ||
| Movements of the Small Intestine | 812 | ||
| Mixing Contractions (Segmentation Contractions) | 812 | ||
| Propulsive Movements | 813 | ||
| Peristalsis in the Small Intestine. | 813 | ||
| Control of Peristalsis by Nervous and Hormonal Signals. | 813 | ||
| Propulsive Effect of the Segmentation Movements. | 813 | ||
| Peristaltic Rush. | 813 | ||
| Movements Caused by the Muscularis Mucosae and Muscle Fibers of the Villi. | 813 | ||
| The Ileocecal Valve Prevents Backflow From the Colon to the Small Intestine | 814 | ||
| Feedback Control of the Ileocecal Sphincter. | 814 | ||
| Movements of the Colon | 814 | ||
| Mixing Movements—“Haustrations.” | 814 | ||
| Propulsive Movements—“Mass Movements.” | 815 | ||
| Initiation of Mass Movements by Gastrocolic and Duodenocolic Reflexes. | 815 | ||
| Defecation | 815 | ||
| Defecation Reflexes. | 815 | ||
| Other Autonomic Reflexes That Affect Bowel Activity | 816 | ||
| Bibliography | 816 | ||
| 65 Secretory Functions of the Alimentary Tract | 817 | ||
| General Principles of Alimentary Tract Secretion | 817 | ||
| Types of Alimentary Tract Glands | 817 | ||
| Basic Mechanisms of Stimulation of the Alimentary Tract Glands | 817 | ||
| Contact of Food with the Epithelium Stimulates Secretion—Function of Enteric Nervous Stimuli | 817 | ||
| Autonomic Stimulation of Secretion | 817 | ||
| Parasympathetic Stimulation Increases the Alimentary Tract Glandular Secretion Rate. | 817 | ||
| Sympathetic Stimulation Has a Dual Effect on the Alimentary Tract Glandular Secretion Rate. | 818 | ||
| Regulation of Glandular Secretion by Hormones. | 818 | ||
| Basic Mechanism of Secretion by Glandular Cells | 818 | ||
| Secretion of Organic Substances. | 818 | ||
| Water and Electrolyte Secretion. | 819 | ||
| Lubricating and Protective Properties of Mucus, and the Importance of Mucus in the Gastrointestinal Tract | 819 | ||
| Secretion of Saliva | 819 | ||
| Saliva Contains a Serous Secretion and a Mucus Secretion. | 819 | ||
| Secretion of Ions in Saliva. | 819 | ||
| Function of Saliva for Oral Hygiene. | 820 | ||
| Nervous Regulation of Salivary Secretion | 820 | ||
| Esophageal Secretion | 821 | ||
| Gastric Secretion | 821 | ||
| Characteristics of the Gastric Secretions | 821 | ||
| Secretions from the Oxyntic (Gastric) Glands | 821 | ||
| Basic Mechanism of Hydrochloric Acid Secretion. | 821 | ||
| The Basic Factors That Stimulate Gastric Secretion Are Acetylcholine, Gastrin, and Histamine. | 822 | ||
| Secretion and Activation of Pepsinogen. | 822 | ||
| Secretion of Intrinsic Factor by Parietal Cells. | 822 | ||
| Pyloric Glands—Secretion of Mucus and Gastrin | 822 | ||
| Surface Mucous Cells | 823 | ||
| Stimulation of Gastric Acid Secretion | 823 | ||
| Parietal Cells of the Oxyntic Glands Are the Only Cells That Secrete Hydrochloric Acid. | 823 | ||
| Stimulation of Acid Secretion by Gastrin. | 823 | ||
| Regulation of Pepsinogen Secretion | 823 | ||
| Phases of Gastric Secretion | 823 | ||
| Cephalic Phase. | 823 | ||
| Gastric Phase. | 823 | ||
| Intestinal Phase. | 824 | ||
| Inhibition of Gastric Secretion by Other Intestinal Factors | 824 | ||
| Gastric Secretion During the Interdigestive Period. | 824 | ||
| Chemical Composition of Gastrin and Other Gastrointestinal Hormones | 824 | ||
| Pancreatic Secretion | 825 | ||
| Pancreatic Digestive Enzymes | 825 | ||
| Secretion of Trypsin Inhibitor Prevents Digestion of the Pancreas. | 825 | ||
| Secretion of Bicarbonate Ions | 825 | ||
| Regulation of Pancreatic Secretion | 826 | ||
| Basic Stimuli That Cause Pancreatic Secretion | 826 | ||
| Multiplicative Effects of Different Stimuli. | 826 | ||
| Phases of Pancreatic Secretion | 826 | ||
| Cephalic and Gastric Phases. | 826 | ||
| Intestinal Phase. | 827 | ||
| Secretin Stimulates Copious Secretion of Bicarbonate Ions, Which Neutralizes Acidic Stomach Chyme. | 827 | ||
| Cholecystokinin Contributes to Control of Digestive Enzyme Secretion by the Pancreas. | 827 | ||
| Bile Secretion by the Liver | 827 | ||
| Physiologic Anatomy of Biliary Secretion | 828 | ||
| Storing and Concentrating Bile in the Gallbladder. | 829 | ||
| Composition of Bile. | 829 | ||
| Cholecystokinin Stimulates Gallbladder Emptying. | 829 | ||
| Function of Bile Salts in Fat Digestion and Absorption | 829 | ||
| Enterohepatic Circulation of Bile Salts. | 830 | ||
| Role of Secretin in Controlling Bile Secretion. | 830 | ||
| Liver Secretion of Cholesterol and Gallstone Formation | 830 | ||
| Secretions of the Small Intestine | 830 | ||
| Secretion of Mucus by Brunner’s Glands in the Duodenum | 830 | ||
| Secretion of Intestinal Digestive Juices by the Crypts of Lieberkühn | 831 | ||
| Mechanism of Secretion of the Watery Fluid. | 831 | ||
| Digestive Enzymes in the Small Intestinal Secretion. | 831 | ||
| Regulation of Small Intestine Secretion—Local Stimuli | 831 | ||
| Secretion of Mucus by the Large Intestine | 831 | ||
| Mucus Secretion. | 831 | ||
| Diarrhea Caused by Excess Secretion of Water and Electrolytes in Response to Irritation. | 832 | ||
| Bibliography | 832 | ||
| 66 Digestion and Absorption in the Gastrointestinal Tract | 833 | ||
| Digestion of the Various Foods by Hydrolysis | 833 | ||
| Hydrolysis of Carbohydrates. | 833 | ||
| Hydrolysis of Fats. | 833 | ||
| Hydrolysis of Proteins. | 833 | ||
| Digestion of Carbohydrates | 833 | ||
| Carbohydrate Foods of the Diet. | 833 | ||
| Digestion of Carbohydrates Begins in the Mouth and Stomach. | 833 | ||
| Digestion of Carbohydrates in the Small Intestine | 834 | ||
| Digestion by Pancreatic Amylase. | 834 | ||
| Hydrolysis of Disaccharides and Small Glucose Polymers Into Monosaccharides by Intestinal Epithelial Enzymes. | 834 | ||
| Digestion of Proteins | 834 | ||
| Proteins of the Diet. | 834 | ||
| Digestion of Proteins in the Stomach. | 834 | ||
| Most Protein Digestion Results From Actions of Pancreatic Proteolytic Enzymes. | 835 | ||
| Digestion of Peptides by Peptidases in the Enterocytes That Line the Small Intestinal Villi. | 835 | ||
| Digestion of Fats | 835 | ||
| Fats of the Diet. | 835 | ||
| Digestion of Fats Occurs Mainly in the Small Intestine. | 836 | ||
| The First Step in Fat Digestion Is Emulsification by Bile Acids and Lecithin. | 836 | ||
| Triglycerides Are Digested by Pancreatic Lipase. | 836 | ||
| End Products of Fat Digestion Are Free Fatty Acids. | 836 | ||
| Bile Salts Form Micelles That Accelerate Fat Digestion. | 836 | ||
| Digestion of Cholesterol Esters and Phospholipids. | 836 | ||
| Basic Principles of Gastrointestinal Absorption | 837 | ||
| Anatomical Basis of Absorption | 837 | ||
| Folds of Kerckring, Villi, and Microvilli Increase the Mucosal Absorptive Area by Nearly 1000-Fold. | 837 | ||
| Absorption in the Small Intestine | 837 | ||
| Isosmotic Absorption of Water | 838 | ||
| Absorption of Ions | 838 | ||
| Sodium Is Actively Transported Through the Intestinal Membrane. | 838 | ||
| Osmosis of the Water. | 839 | ||
| Aldosterone Greatly Enhances Sodium Absorption. | 839 | ||
| Absorption of Chloride Ions in the Small Intestine. | 839 | ||
| Absorption of Bicarbonate Ions in the Duodenum and Jejunum. | 839 | ||
| Secretion of Bicarbonate and Absorption of Chloride Ions in the Ileum and Large Intestine. | 840 | ||
| Extreme Secretion of Chloride Ions, Sodium Ions, and Water from the Large Intestine Epithelium in Some Types of Diarrhea. | 840 | ||
| Active Absorption of Calcium, Iron, Potassium, Magnesium, and Phosphate. | 840 | ||
| Absorption of Nutrients | 840 | ||
| Carbohydrates Are Mainly Absorbed as Monosaccharides | 840 | ||
| Glucose Is Transported by a Sodium Co-Transport Mechanism. | 840 | ||
| Absorption of Other Monosaccharides. | 841 | ||
| Absorption of Proteins as Dipeptides, Tripeptides, or Amino Acids | 841 | ||
| Absorption of Fats | 841 | ||
| Direct Absorption of Fatty Acids Into the Portal Blood. | 841 | ||
| Absorption in the Large Intestine: Formation of Feces | 841 | ||
| Absorption and Secretion of Electrolytes and Water. | 842 | ||
| Maximum Absorption Capacity of the Large Intestine. | 842 | ||
| Bacterial Action in the Colon. | 842 | ||
| Composition of the Feces. | 842 | ||
| Bibliography | 842 | ||
| 67 Physiology of Gastrointestinal Disorders | 843 | ||
| Disorders of Swallowing and the Esophagus | 843 | ||
| Paralysis of the Swallowing Mechanism. | 843 | ||
| Achalasia and Megaesophagus. | 843 | ||
| Disorders of the Stomach | 843 | ||
| Gastritis—Inflammation of the Gastric Mucosa | 843 | ||
| Gastric Barrier and Its Penetration in Gastritis. | 843 | ||
| Chronic Gastritis Can Lead to Gastric Atrophy and Loss of Stomach Secretions | 844 | ||
| Achlorhydria (and Hypochlorhydria). | 844 | ||
| Gastric Atrophy May Cause Pernicious Anemia. | 844 | ||
| Peptic Ulcer | 844 | ||
| Basic Cause of Peptic Ulceration. | 844 | ||
| Specific Causes of Peptic Ulcer | 845 | ||
| Bacterial Infection by Helicobacter pylori Breaks Down the Gastroduodenal Mucosal Barrier and Stimulates Gastric Acid Secretion. | 845 | ||
| Other Causes of Ulceration. | 845 | ||
| Treatment of Peptic Ulcers. | 845 | ||
| Disorders of the Small Intestine | 845 | ||
| Abnormal Digestion of Food in the Small Intestine—Pancreatic Failure | 845 | ||
| Pancreatitis—Inflammation of the Pancreas. | 845 | ||
| Malabsorption by the Small Intestinal Mucosa—Sprue | 845 | ||
| Nontropical Sprue. | 845 | ||
| Tropical Sprue. | 846 | ||
| Malabsorption in Sprue. | 846 | ||
| Disorders of the Large Intestine | 846 | ||
| Constipation | 846 | ||
| Megacolon (Hirschsprung’s Disease). | 846 | ||
| Diarrhea | 846 | ||
| Enteritis—Inflammation of the Intestinal Tract. | 846 | ||
| Psychogenic Diarrhea. | 846 | ||
| Ulcerative Colitis. | 847 | ||
| Paralysis of Defecation in Persons With Spinal Cord Injuries | 847 | ||
| General Disorders of the Gastrointestinal Tract | 847 | ||
| Vomiting | 847 | ||
| Antiperistalsis, the Prelude to Vomiting. | 847 | ||
| Vomiting Act. | 848 | ||
| Chemoreceptor “Trigger Zone” in the Brain Medulla for Initiation of Vomiting by Drugs or by Motion Sickness. | 848 | ||
| Nausea | 848 | ||
| Gastrointestinal Obstruction | 848 | ||
| Gases in the Gastrointestinal Tract (Flatus) | 848 | ||
| Bibliography | 849 | ||
| Unit XIII Metabolism and Temperature Regulation | 851 | ||
| 68 Metabolism of Carbohydrates and Formation of Adenosine Triphosphate | 853 | ||
| Release of Energy From Foods and “Free Energy” | 853 | ||
| Coupled Reactions. | 853 | ||
| “Free Energy.” | 853 | ||
| Adenosine Triphosphate Is the “Energy Currency” of the Body | 853 | ||
| Central Role of Glucose in Carbohydrate Metabolism | 854 | ||
| Transport of Glucose Through the Cell Membrane | 854 | ||
| Insulin Increases Facilitated Diffusion of Glucose | 855 | ||
| Phosphorylation of Glucose | 855 | ||
| Glycogen Is Stored in the Liver and Muscle | 855 | ||
| Glycogenesis—Formation of Glycogen | 855 | ||
| Glycogenolysis—Breakdown of Stored Glycogen | 856 | ||
| Activation of Phosphorylase by Epinephrine or by Glucagon. | 856 | ||
| Release of Energy From Glucose by the Glycolytic Pathway | 856 | ||
| Glycolysis—Splitting Glucose to Form Pyruvic Acid | 856 | ||
| Formation of ATP During Glycolysis. | 856 | ||
| Conversion of Pyruvic Acid to Acetyl Coenzyme A | 857 | ||
| Citric Acid Cycle (Krebs Cycle) | 857 | ||
| Formation of ATP in the Citric Acid Cycle. | 858 | ||
| Function of Dehydrogenases and Nicotinamide Adenine Dinucleotide in Causing Release of Hydrogen Atoms in the Citric Acid Cycle. | 858 | ||
| Function of Decarboxylases in Causing Release of Carbon Dioxide. | 858 | ||
| Formation of Large Quantities of ATP by Oxidation of Hydrogen—The Process of Oxidative Phosphorylation | 858 | ||
| Chemiosmotic Mechanism of the Mitochondria to Form ATP | 859 | ||
| Ionization of Hydrogen, the Electron Transport Chain, and Formation of Water. | 859 | ||
| Pumping of Hydrogen Ions Into the Outer Chamber of the Mitochondrion, Caused by the Electron Transport Chain. | 859 | ||
| Formation of ATP. | 859 | ||
| Summary of ATP Formation During the Breakdown of Glucose | 859 | ||
| Effect of ATP and ADP Cell Concentrations in Controlling Glycolysis and Glucose Oxidation | 859 | ||
| Anaerobic Release of Energy— Anaerobic Glycolysis | 860 | ||
| Formation of Lactic Acid During Anaerobic Glycolysis Allows Release of Extra Anaerobic Energy. | 860 | ||
| Reconversion of Lactic Acid to Pyruvic Acid When Oxygen Becomes Available Again. | 860 | ||
| Use of Lactic Acid by the Heart for Energy. | 860 | ||
| Release of Energy From Glucose by the Pentose Phosphate Pathway | 861 | ||
| Release of Carbon Dioxide and Hydrogen by the Pentose Phosphate Pathway. | 861 | ||
| Use of Hydrogen to Synthesize Fat; the Function of Nicotinamide Adenine Dinucleotide Phosphate. | 861 | ||
| Glucose Conversion to Glycogen or Fat | 861 | ||
| Formation of Carbohydrates From Proteins and Fats—Gluconeogenesis | 861 | ||
| Regulation of Gluconeogenesis | 862 | ||
| Effect of Corticotropin and Glucocorticoids on Gluconeogenesis. | 862 | ||
| Blood Glucose | 862 | ||
| Bibliography | 862 | ||
| 69 Lipid Metabolism | 863 | ||
| Basic Chemical Structure of Triglycerides (Neutral Fat) | 863 | ||
| Transport of Lipids in the Body Fluids | 863 | ||
| Transport of Triglycerides and Other Lipids From the Gastrointestinal Tract by Lymph—the Chylomicrons | 863 | ||
| Removal of the Chylomicrons From the Blood | 863 | ||
| Chylomicron Triglycerides Are Hydrolyzed by Lipoprotein Lipase, and Fat Is Stored in Adipose Tissue. | 864 | ||
| “Free Fatty Acids” Are Transported in the Blood in Combination With Albumin | 864 | ||
| Lipoproteins—Their Special Function in Transporting Cholesterol and Phospholipids | 865 | ||
| Types of Lipoproteins. | 865 | ||
| Formation and Function of Lipoproteins. | 865 | ||
| Fat Deposits | 865 | ||
| Adipose Tissue | 865 | ||
| Fat Cells (Adipocytes) Store Triglycerides. | 865 | ||
| Tissue Lipases Permit Exchange of Fat Between Adipose Tissue and the Blood. | 866 | ||
| Liver Lipids | 866 | ||
| Use of Triglycerides for Energy: Formation of Adenosine Triphosphate | 866 | ||
| Hydrolysis of Triglycerides Into Fatty Acids and Glycerol. | 866 | ||
| Entry of Fatty Acids Into Mitochondria. | 866 | ||
| Degradation of Fatty Acids to Acetyl Coenzyme A by Beta-Oxidation. | 866 | ||
| Oxidation of Acetyl-CoA. | 867 | ||
| Large Amounts of ATP Are Formed by Oxidation of Fatty Acids. | 867 | ||
| Formation of Acetoacetic Acid in the Liver and Its Transport in the Blood | 867 | ||
| Ketosis in Starvation, Diabetes, and Other Diseases. | 868 | ||
| Adaptation to a High-Fat Diet. | 868 | ||
| Synthesis of Triglycerides From Carbohydrates | 868 | ||
| Conversion of Acetyl-CoA Into Fatty Acids. | 868 | ||
| Combination of Fatty Acids With α-Glycerophosphate to Form Triglycerides | 868 | ||
| Efficiency of Carbohydrate Conversion Into Fat. | 868 | ||
| Importance of Fat Synthesis and Storage. | 869 | ||
| Failure to Synthesize Fats From Carbohydrates in the Absence of Insulin. | 869 | ||
| Synthesis of Triglycerides From Proteins | 869 | ||
| Regulation of Energy Release From Triglycerides | 869 | ||
| Carbohydrates Are Preferred Over Fats for Energy When Excess Carbohydrates Are Available. | 869 | ||
| Acceleration of Fat Utilization for Energy in the Absence of Carbohydrates. | 869 | ||
| Hormonal Regulation of Fat Utilization. | 870 | ||
| Obesity—Excess Deposition of Fat | 870 | ||
| Phospholipids and Cholesterol | 870 | ||
| Phospholipids | 870 | ||
| Formation of Phospholipids. | 871 | ||
| Specific Uses of Phospholipids. | 871 | ||
| Cholesterol | 871 | ||
| Formation of Cholesterol. | 871 | ||
| Factors That Affect Plasma Cholesterol Concentration—Feedback Control of Body Cholesterol. | 871 | ||
| Specific Uses of Cholesterol in the Body. | 872 | ||
| Cellular Structural Functions of Phospholipids and Cholesterol—Especially for Membranes | 872 | ||
| Atherosclerosis | 872 | ||
| Roles of Cholesterol and Lipoproteins in Atherosclerosis | 872 | ||
| Increased Low-Density Lipoproteins. | 872 | ||
| Familial Hypercholesterolemia. | 873 | ||
| Role of High-Density Lipoproteins in Preventing Atherosclerosis. | 873 | ||
| Other Major Risk Factors for Atherosclerosis | 873 | ||
| Prevention of Atherosclerosis | 874 | ||
| Bibliography | 874 | ||
| 70 Protein Metabolism | 875 | ||
| Basic Properties of Proteins | 875 | ||
| Amino Acids Are the Principal Constituents of Proteins | 875 | ||
| Peptide Linkages and Peptide Chains. | 875 | ||
| Other Linkages in Protein Molecules. | 875 | ||
| Transport and Storage of Amino Acids | 875 | ||
| Blood Amino Acids | 875 | ||
| Fate of Amino Acids Absorbed From the Gastrointestinal Tract. | 876 | ||
| Active Transport of Amino Acids Into the Cells. | 876 | ||
| Renal Threshold for Amino Acids. | 877 | ||
| Storage of Amino Acids as Proteins in the Cells | 877 | ||
| Release of Amino Acids From the Cells as a Means of Regulating Plasma Amino Acid Concentration. | 877 | ||
| Reversible Equilibrium Between the Proteins in Different Parts of the Body. | 877 | ||
| Upper Limit for the Storage of Proteins. | 877 | ||
| Functional Roles of the Plasma Proteins | 877 | ||
| Formation of the Plasma Proteins. | 877 | ||
| Plasma Proteins as a Source of Amino Acids for the Tissues. | 878 | ||
| Reversible Equilibrium Between the Plasma Proteins and the Tissue Proteins. | 878 | ||
| Essential and Nonessential Amino Acids. | 878 | ||
| Use of Proteins for Energy | 878 | ||
| Deamination—the Removal of Amino Groups From Amino Acids. | 878 | ||
| Urea Formation by the Liver. | 879 | ||
| Oxidation of Deaminated Amino Acids. | 879 | ||
| Gluconeogenesis and Ketogenesis. | 879 | ||
| Obligatory Degradation of Proteins | 879 | ||
| Effect of Starvation on Protein Degradation. | 879 | ||
| Hormonal Regulation of Protein Metabolism | 880 | ||
| Growth Hormone Increases the Synthesis of Cellular Proteins. | 880 | ||
| Insulin Is Necessary for Protein Synthesis. | 880 | ||
| Glucocorticoids Increase Breakdown of Most Tissue Proteins. | 880 | ||
| Testosterone Increases Protein Deposition in Tissues. | 880 | ||
| Estrogen. | 880 | ||
| Thyroxine Increases Metabolism of Cells. | 880 | ||
| Bibliography | 880 | ||
| 71 The Liver as an Organ | 881 | ||
| Physiological Anatomy of the Liver | 881 | ||
| Hepatic Vascular and Lymph Systems | 881 | ||
| Blood Flows Through the Liver From the Portal Vein and Hepatic Artery | 881 | ||
| The Liver Has High Blood Flow and Low Vascular Resistance. | 881 | ||
| Cirrhosis of the Liver Greatly Increases Resistance to Blood Flow. | 881 | ||
| The Liver Functions as a Blood Reservoir | 882 | ||
| The Liver Has Very High Lymph Flow | 882 | ||
| High Hepatic Vascular Pressures Can Cause Fluid Transudation Into the Abdominal Cavity From the Liver and Portal Capillaries—Ascites. | 882 | ||
| Regulation of Liver Mass—Regeneration | 882 | ||
| The Hepatic Macrophage System Serves a Blood-Cleansing Function | 883 | ||
| Metabolic Functions of the Liver | 883 | ||
| Carbohydrate Metabolism | 883 | ||
| Fat Metabolism | 883 | ||
| Protein Metabolism | 883 | ||
| Other Metabolic Functions of the Liver | 884 | ||
| The Liver Is a Storage Site for Vitamins. | 884 | ||
| The Liver Stores Iron as Ferritin. | 884 | ||
| The Liver Forms Blood Substances Used in Coagulation. | 884 | ||
| The Liver Removes or Excretes Drugs, Hormones, and Other Substances. | 884 | ||
| Measurement of Bilirubin in the Bile as a Clinical Diagnostic Tool | 884 | ||
| Formation and Fate of Urobilinogen. | 885 | ||
| Jaundice—Excess Bilirubin in the Extracellular Fluid | 885 | ||
| Hemolytic Jaundice Is Caused by Hemolysis of Red Blood Cells. | 886 | ||
| Obstructive Jaundice Is Caused by Obstruction of Bile Ducts or Liver Disease. | 886 | ||
| Diagnostic Differences Between Hemolytic and Obstructive Jaundice. | 886 | ||
| Bibliography | 886 | ||
| 72 Dietary Balances; Regulation of Feeding; Obesity and Starvation; Vitamins and Minerals | 887 | ||
| Energy Intake and Output are Balanced Under Steady-State Conditions | 887 | ||
| Dietary Balances | 887 | ||
| Energy Available in Foods | 887 | ||
| The Average Daily Requirement for Protein Is 30 to 50 Grams. | 887 | ||
| Carbohydrates and Fats Act as “Protein Sparers.” | 887 | ||
| Methods for Determining Metabolic Utilization of Carbohydrates, Fats, and Proteins | 888 | ||
| “Respiratory Quotient,” the Ratio of Carbon Dioxide Production to Oxygen Utilization, Can Be Used to Estimate Fat and Carbohydrate Utilization. | 888 | ||
| Nitrogen Excretion Can Be Used to Assess Protein Metabolism. | 889 | ||
| Regulation of Food Intake and Energy Storage | 889 | ||
| Neural Centers Regulate Food Intake | 889 | ||
| The Hypothalamus Contains Hunger and Satiety Centers. | 889 | ||
| Neurons and Neurotransmitters in the Hypothalamus That Stimulate or Inhibit Feeding. | 890 | ||
| Neural Centers That Influence the Mechanical Process of Feeding. | 892 | ||
| Factors That Regulate Quantity of Food Intake | 892 | ||
| Short-Term Regulation of Food Intake | 892 | ||
| Gastrointestinal Filling Inhibits Feeding. | 892 | ||
| Gastrointestinal Hormonal Factors Suppress Feeding. | 892 | ||
| Ghrelin, a Gastrointestinal Hormone, Increases Feeding. | 892 | ||
| Oral Receptors Meter Food Intake. | 893 | ||
| Intermediate- and Long-Term Regulation of Food Intake | 893 | ||
| Effect of Blood Concentrations of Glucose, Amino Acids, and Lipids on Hunger and Feeding. | 893 | ||
| Temperature Regulation and Food Intake. | 893 | ||
| Feedback Signals From Adipose Tissue Regulate Food Intake. | 893 | ||
| Summary of Long-Term Regulation. | 894 | ||
| Importance of Having Both Long- and Short-Term Regulatory Systems for Feeding | 894 | ||
| Obesity | 894 | ||
| Obesity Results From Greater Intake Than Expenditure of Energy | 894 | ||
| Decreased Physical Activity and Abnormal Feeding Regulation as Causes of Obesity | 894 | ||
| Sedentary Lifestyle Is a Major Cause of Obesity. | 895 | ||
| Abnormal Feeding Behavior Is an Important Cause of Obesity. | 895 | ||
| Childhood Overnutrition as a Possible Cause of Obesity. | 895 | ||
| Neurogenic Abnormalities as a Cause of Obesity. | 895 | ||
| Genetic Factors as a Cause of Obesity. | 895 | ||
| Treatment of Obesity | 895 | ||
| Inanition, Anorexia, and Cachexia | 896 | ||
| Starvation | 897 | ||
| Depletion of Food Stores in the Body Tissues During Starvation. | 897 | ||
| Vitamin Deficiencies in Starvation. | 897 | ||
| Vitamins | 897 | ||
| Daily Requirements of Vitamins. | 897 | ||
| Storage of Vitamins in the Body. | 897 | ||
| Vitamin A | 898 | ||
| Vitamin A Deficiency Causes “Night Blindness” and Abnormal Epithelial Cell Growth. | 898 | ||
| Thiamine (Vitamin B1) | 898 | ||
| Thiamine Deficiency Causes Lesions of the Central and Peripheral Nervous Systems. | 898 | ||
| Thiamine Deficiency Weakens the Heart and Causes Peripheral Vasodilation. | 898 | ||
| Thiamine Deficiency Causes Gastrointestinal Tract Disturbances. | 898 | ||
| Niacin | 898 | ||
| Riboflavin (Vitamin B2) | 899 | ||
| Vitamin B12 | 899 | ||
| Vitamin B12 Deficiency Causes Pernicious Anemia. | 899 | ||
| Vitamin B12 Deficiency Causes Demyelination of the Large Nerve Fibers of the Spinal Cord. | 899 | ||
| Folic Acid (Pteroylglutamic Acid) | 899 | ||
| Pyridoxine (Vitamin B6) | 899 | ||
| Pantothenic Acid | 899 | ||
| Ascorbic Acid (Vitamin C) | 900 | ||
| Ascorbic Acid Deficiency Weakens Collagen Fibers Throughout the Body. | 900 | ||
| Ascorbic Acid Deficiency Causes Scurvy. | 900 | ||
| Vitamin D | 900 | ||
| Vitamin E | 900 | ||
| Vitamin K | 900 | ||
| Mineral Metabolism | 900 | ||
| Magnesium. | 900 | ||
| Calcium. | 901 | ||
| Phosphorus. | 901 | ||
| Iron. | 901 | ||
| Important Trace Elements in the Body. | 901 | ||
| Iodine. | 901 | ||
| Zinc. | 901 | ||
| Fluorine. | 901 | ||
| Bibliography | 902 | ||
| 73 Energetics and Metabolic Rate | 903 | ||
| Adenosine Triphosphate Functions as an “Energy Currency” in Metabolism | 903 | ||
| ATP Is Generated by Combustion of Carbohydrates, Fats, and Proteins. | 903 | ||
| ATP Energizes the Synthesis of Cellular Components. | 903 | ||
| ATP Energizes Muscle Contraction. | 903 | ||
| ATP Energizes Active Transport Across Membranes. | 903 | ||
| ATP Energizes Glandular Secretion. | 903 | ||
| ATP Energizes Nerve Conduction. | 904 | ||
| Phosphocreatine Functions as an Accessory Storage Depot for Energy and as an “ATP Buffer” | 904 | ||
| Anaerobic Versus Aerobic Energy | 904 | ||
| Anaerobic Energy Utilization During Hypoxia. | 904 | ||
| Anaerobic Energy Utilization During Strenuous Bursts of Activity Is Derived Mainly From Glycolysis. | 904 | ||
| Extra Consumption of Oxygen Repays the Oxygen Debt After Completion of Strenuous Exercise. | 905 | ||
| Summary of Energy Utilization by the Cells | 905 | ||
| Control of Energy Release in the Cell | 905 | ||
| Rate Control of Enzyme-Catalyzed Reactions. | 905 | ||
| Role of Enzyme Concentration in Regulation of Metabolic Reactions. | 906 | ||
| Role of Substrate Concentration in Regulation of Metabolic Reactions. | 906 | ||
| Rate Limitation in a Series of Reactions. | 906 | ||
| ADP Concentration as a Rate-Controlling Factor in Energy Release. | 906 | ||
| Metabolic Rate | 906 | ||
| Heat Is the End Product of Almost All the Energy Released in the Body. | 906 | ||
| The Calorie. | 906 | ||
| Measurement of the Whole-Body Metabolic Rate | 907 | ||
| Direct Calorimetry Measures Heat Liberated From the Body. | 907 | ||
| Indirect Calorimetry—The “Energy Equivalent” of Oxygen. | 907 | ||
| Energy Metabolism—Factors That Influence Energy Output | 907 | ||
| Overall Energy Requirements for Daily Activities | 907 | ||
| Basal Metabolic Rate—The Minimum Energy Expenditure for the Body to Exist | 907 | ||
| Thyroid Hormone Increases Metabolic Rate. | 908 | ||
| Male Sex Hormone Increases Metabolic Rate. | 908 | ||
| Growth Hormone Increases Metabolic Rate. | 908 | ||
| Fever Increases Metabolic Rate. | 908 | ||
| Sleep Decreases Metabolic Rate. | 908 | ||
| Malnutrition Decreases Metabolic Rate. | 908 | ||
| Energy Used for Physical Activities | 908 | ||
| Energy Used for Processing Food—Thermogenic Effect of Food | 909 | ||
| Energy Used for Nonshivering Thermogenesis—Role of Sympathetic Stimulation | 909 | ||
| Bibliography | 909 | ||
| 74 Body Temperature Regulation and Fever | 911 | ||
| Normal Body Temperatures | 911 | ||
| Body Core Temperature and Skin Temperature. | 911 | ||
| Normal Core Temperature. | 911 | ||
| Body Temperature is Controlled by Balancing Heat Production and Heat Loss | 911 | ||
| Heat Production | 911 | ||
| Heat Loss | 911 | ||
| Insulator System of the Body | 911 | ||
| Blood Flow to the Skin From the Body Core Provides Heat Transfer | 912 | ||
| Control of Heat Conduction to the Skin by the Sympathetic Nervous System. | 912 | ||
| Basic Physics of How Heat Is Lost From the Skin Surface | 912 | ||
| Radiation Causes Heat Loss in the Form of Infrared Rays. | 912 | ||
| Conductive Heat Loss Occurs by Direct Contact With an Object. | 913 | ||
| Convective Heat Loss Results From Air Movement. | 913 | ||
| Cooling Effect of Wind. | 913 | ||
| Conduction and Convection of Heat From a Person Suspended in Water. | 913 | ||
| Evaporation. | 913 | ||
| Evaporation Is a Necessary Cooling Mechanism at Very High Air Temperatures. | 913 | ||
| Clothing Reduces Conductive and Convective Heat Loss. | 913 | ||
| Sweating and Its Regulation by the Autonomic Nervous System | 914 | ||
| Mechanism of Sweat Secretion. | 914 | ||
| Acclimatization of the Sweating Mechanism to Heat—The Role of Aldosterone. | 915 | ||
| Loss of Heat by Panting | 915 | ||
| Regulation of Body Temperature—Role of the Hypothalamus | 915 | ||
| Role of the Anterior Hypothalamic-Preoptic Area in Thermostatic Detection of Temperature | 916 | ||
| Detection of Temperature by Receptors in the Skin and Deep Body Tissues | 916 | ||
| Posterior Hypothalamus Integrates the Central and Peripheral Temperature Sensory Signals | 916 | ||
| Neuronal Effector Mechanisms That Decrease or Increase Body Temperature | 916 | ||
| Temperature-Decreasing Mechanisms When the Body Is Too Hot | 916 | ||
| Temperature-Increasing Mechanisms When the Body Is Too Cold | 917 | ||
| Hypothalamic Stimulation of Shivering. | 917 | ||
| Sympathetic “Chemical” Excitation of Heat Production. | 917 | ||
| Increased Thyroxine Output as a Long-Term Cause of Increased Heat Production. | 918 | ||
| “Set Point” for Temperature Control | 918 | ||
| Feedback Gain for Body Temperature Control. | 918 | ||
| Skin Temperature Can Slightly Alter the Set Point for Core Temperature Control | 918 | ||
| Behavioral Control of Body Temperature | 919 | ||
| Local Skin Temperature Reflexes | 919 | ||
| Regulation of Internal Body Temperature Is Impaired by Cutting the Spinal Cord. | 919 | ||
| Abnormalities of Body Temperature Regulation | 919 | ||
| Fever | 919 | ||
| Resetting the Hypothalamic Temperature-Regulating Center in Febrile Diseases—Effect of Pyrogens | 920 | ||
| Mechanism of Action of Pyrogens in Causing Fever—Role of Cytokines. | 920 | ||
| Fever Caused by Brain Lesions. | 920 | ||
| Characteristics of Febrile Conditions | 920 | ||
| Chills. | 920 | ||
| Crisis, or “Flush.” | 921 | ||
| Heatstroke | 921 | ||
| Harmful Effects of High Temperature. | 921 | ||
| Acclimatization to Heat. | 921 | ||
| Exposure of the Body to Extreme Cold | 921 | ||
| Loss of Temperature Regulation at Low Temperatures. | 921 | ||
| Frostbite. | 921 | ||
| Cold-Induced Vasodilation Is a Final Protection Against Frostbite at Almost Freezing Temperatures. | 921 | ||
| Artificial Hypothermia. | 922 | ||
| Bibliography | 922 | ||
| Unit XIV Endocrinology and Reproduction | 923 | ||
| 75 Introduction to Endocrinology | 925 | ||
| Coordination of Body Functions by Chemical Messengers | 925 | ||
| Chemical Structure and Synthesis of Hormones | 925 | ||
| Polypeptide and Protein Hormones Are Stored in Secretory Vesicles Until Needed. | 926 | ||
| Steroid Hormones Are Usually Synthesized From Cholesterol and Are Not Stored. | 928 | ||
| Amine Hormones Are Derived From Tyrosine. | 928 | ||
| Hormone Secretion, Transport, and Clearance From the Blood | 929 | ||
| Hormone Secretion After a Stimulus and Duration of Action of Different Hormones. | 929 | ||
| Concentrations of Hormones in the Circulating Blood and Hormonal Secretion Rates. | 929 | ||
| Feedback Control of Hormone Secretion | 929 | ||
| Negative Feedback Prevents Overactivity of Hormone Systems. | 929 | ||
| Surges of Hormones Can Occur With Positive Feedback. | 929 | ||
| Cyclical Variations Occur in Hormone Release. | 929 | ||
| Transport of Hormones in the Blood | 929 | ||
| “Clearance” of Hormones From the Blood. | 929 | ||
| Mechanisms of Action of Hormones | 930 | ||
| Hormone Receptors and Their Activation | 930 | ||
| The Number and Sensitivity of Hormone Receptors Are Regulated. | 930 | ||
| Intracellular Signaling after Hormone Receptor Activation | 931 | ||
| Ion Channel–Linked Receptors. | 931 | ||
| G Protein–Linked Hormone Receptors. | 931 | ||
| Enzyme-Linked Hormone Receptors. | 932 | ||
| Intracellular Hormone Receptors and Activation of Genes. | 933 | ||
| Second Messenger Mechanisms for Mediating Intracellular Hormonal Functions | 933 | ||
| Adenylyl Cyclase–cAMP Second Messenger System | 933 | ||
| Cell Membrane Phospholipid Second Messenger System | 934 | ||
| Calcium-Calmodulin Second Messenger System | 934 | ||
| Hormones That Act Mainly on the Genetic Machinery of the Cell | 935 | ||
| Steroid Hormones Increase Protein Synthesis | 935 | ||
| Thyroid Hormones Increase Gene Transcription in the Cell Nucleus | 935 | ||
| Measurement of Hormone Concentrations in the Blood | 936 | ||
| Radioimmunoassay | 936 | ||
| Enzyme-Linked Immunosorbent Assay | 936 | ||
| Bibliography | 937 | ||
| 76 Pituitary Hormones and Their Control by the Hypothalamus | 939 | ||
| Pituitary Gland and Its Relation to the Hypothalamus | 939 | ||
| The Anterior and Posterior Lobes of the Pituitary Gland | 939 | ||
| The Anterior Pituitary Gland Contains Several Different Cell Types That Synthesize and Secrete Hormones. | 939 | ||
| Posterior Pituitary Hormones Are Synthesized by Cell Bodies in the Hypothalamus. | 940 | ||
| Hypothalamus Controls Pituitary Secretion | 940 | ||
| Hypothalamic-Hypophysial Portal Blood Vessels of the Anterior Pituitary Gland | 941 | ||
| Hypothalamic Releasing and Inhibitory Hormones Are Secreted Into the Median Eminence. | 941 | ||
| Hypothalamic Releasing and Inhibitory Hormones Control Anterior Pituitary Secretion. | 941 | ||
| Specific Areas in the Hypothalamus Control Secretion of Specific Hypothalamic Releasing and Inhibitory Hormones. | 942 | ||
| Physiological Functions of Growth Hormone | 942 | ||
| Growth Hormone Promotes Growth of Many Body Tissues | 942 | ||
| Growth Hormone Has Several Metabolic Effects | 943 | ||
| Growth Hormone Promotes Protein Deposition in Tissues | 943 | ||
| Enhancement of Amino Acid Transport Through the Cell Membranes. | 943 | ||
| Enhancement of RNA Translation to Cause Protein Synthesis by the Ribosomes. | 943 | ||
| Increased Nuclear Transcription of DNA to Form RNA. | 943 | ||
| Decreased Catabolism of Protein and Amino Acids. | 943 | ||
| Summary. | 943 | ||
| Growth Hormone Enhances Fat Utilization for Energy | 943 | ||
| “Ketogenic” Effect of Excessive Growth Hormone. | 943 | ||
| Growth Hormone Decreases Carbohydrate Utilization | 943 | ||
| Necessity of Insulin and Carbohydrate for the Growth-Promoting Action of Growth Hormone | 944 | ||
| Growth Hormone Stimulates Cartilage and Bone Growth | 944 | ||
| Growth Hormone Exerts Much of Its Effect Through Intermediate Substances Called Somatomedins | 944 | ||
| Short Duration of Action of Growth Hormone but Prolonged Action of Somatomedin C. | 945 | ||
| Regulation of Growth Hormone Secretion | 945 | ||
| Role of the Hypothalamus, Growth Hormone–Releasing Hormone, and Somatostatin in Controlling Growth Hormone Secretion | 946 | ||
| Abnormalities of Growth Hormone Secretion | 946 | ||
| Panhypopituitarism. | 946 | ||
| Panhypopituitarism in the Adult. | 947 | ||
| Dwarfism. | 947 | ||
| Treatment with Human Growth Hormone. | 947 | ||
| Gigantism. | 947 | ||
| Acromegaly. | 947 | ||
| Possible Role of Decreased Growth Hormone Secretion in Causing Changes Associated with Aging | 947 | ||
| Posterior Pituitary Gland and Its Relation to the Hypothalamus | 948 | ||
| Chemical Structures of Antidiuretic Hormone and Oxytocin | 949 | ||
| Physiological Functions of Antidiuretic Hormone | 949 | ||
| Regulation of Antidiuretic Hormone Production | 949 | ||
| Increased Extracellular Fluid Osmolarity Stimulates ADH Secretion. | 949 | ||
| Low Blood Volume and Low Blood Pressure Stimulate ADH Secretion—Vasoconstrictor Effects of ADH. | 949 | ||
| Physiological Functions of Oxytocin | 950 | ||
| Oxytocin Causes Contraction of the Pregnant Uterus. | 950 | ||
| Oxytocin Aids in Milk Ejection by the Breasts. | 950 | ||
| Bibliography | 950 | ||
| 77 Thyroid Metabolic Hormones | 951 | ||
| Synthesis and Secretion of the Thyroid Metabolic Hormones | 951 | ||
| Physiological Anatomy of the Thyroid Gland | 951 | ||
| Iodine is Required for Formation of Thyroxine | 951 | ||
| Fate of Ingested Iodides. | 951 | ||
| Iodide Pump—the Sodium-Iodide Symporter (Iodide Trapping) | 951 | ||
| Thyroglobulin and Chemistry of Thyroxine and Triiodothyronine Formation | 952 | ||
| Formation and Secretion of Thyroglobulin by the Thyroid Cells. | 952 | ||
| Oxidation of the Iodide Ion. | 953 | ||
| Iodination of Tyrosine and Formation of the Thyroid Hormones—“Organification” of Thyroglobulin. | 953 | ||
| Storage of Thyroglobulin. | 953 | ||
| Release of Thyroxine and Triiodothyronine From the Thyroid Gland | 953 | ||
| Daily Rate of Secretion of Thyroxine and Triiodothyronine. | 954 | ||
| Transport of Thyroxine and Triiodothyronine to Tissues | 954 | ||
| Thyroxine and Triiodothyronine Are Bound to Plasma Proteins. | 954 | ||
| Thyroxine and Triiodothyronine Are Released Slowly to Tissue Cells. | 954 | ||
| Thyroid Hormones Have Slow Onset and Long Duration of Action. | 954 | ||
| Physiological Functions of the Thyroid Hormones | 954 | ||
| Thyroid Hormones Increase Transcription of Large Numbers of Genes | 954 | ||
| Most of the Thyroxine Secreted by the Thyroid Is Converted to Triiodothyronine. | 954 | ||
| Thyroid Hormones Activate Nuclear Receptors. | 955 | ||
| Thyroid Hormones Increase Cellular Metabolic Activity | 956 | ||
| Thyroid Hormones Increase the Number and Activity of Mitochondria. | 956 | ||
| Thyroid Hormones Increase Active Transport of Ions Through Cell Membranes. | 956 | ||
| Effect of Thyroid Hormone on Growth | 956 | ||
| Effects of Thyroid Hormone on Specific Body Functions | 956 | ||
| Stimulation of Carbohydrate Metabolism. | 956 | ||
| Stimulation of Fat Metabolism. | 956 | ||
| Effect on Plasma and Liver Fats. | 956 | ||
| Increased Requirement for Vitamins. | 957 | ||
| Increased Basal Metabolic Rate. | 957 | ||
| Decreased Body Weight. | 957 | ||
| Increased Blood Flow and Cardiac Output. | 957 | ||
| Increased Heart Rate. | 957 | ||
| Increased Heart Strength. | 957 | ||
| Normal Arterial Pressure. | 957 | ||
| Increased Respiration. | 957 | ||
| Increased Gastrointestinal Motility. | 957 | ||
| Excitatory Effects on the Central Nervous System. | 958 | ||
| Effect on the Function of the Muscles. | 958 | ||
| Muscle Tremor. | 958 | ||
| Effect on Sleep. | 958 | ||
| Effect on Other Endocrine Glands. | 958 | ||
| Effect of Thyroid Hormone on Sexual Function. | 958 | ||
| Regulation of Thyroid Hormone Secretion | 958 | ||
| TSH (From the Anterior Pituitary Gland) Increases Thyroid Secretion | 958 | ||
| Cyclic Adenosine Monophosphate Mediates the Stimulatory Effect of TSH. | 959 | ||
| Anterior Pituitary Secretion of TSH is Regulated by Thyrotropin-Releasing Hormone From the Hypothalamus | 959 | ||
| Effects of Cold and Other Neurogenic Stimuli on TRH and TSH Secretion. | 959 | ||
| Feedback Effect of Thyroid Hormone to Decrease Anterior Pituitary Secretion of TSH | 959 | ||
| Antithyroid Substances Suppress Thyroid Secretion | 959 | ||
| Thiocyanate Ions Decrease Iodide Trapping. | 960 | ||
| Propylthiouracil Decreases Thyroid Hormone Formation. | 960 | ||
| Iodides in High Concentrations Decrease Thyroid Activity and Thyroid Gland Size. | 960 | ||
| Diseases of the Thyroid | 960 | ||
| Hyperthyroidism | 960 | ||
| Causes of Hyperthyroidism (Toxic Goiter, Thyrotoxicosis, Graves’ Disease). | 960 | ||
| Thyroid Adenoma. | 960 | ||
| Symptoms of Hyperthyroidism | 961 | ||
| Exophthalmos. | 961 | ||
| Diagnostic Tests for Hyperthyroidism. | 961 | ||
| Treatment in Hyperthyroidism. | 961 | ||
| Treatment of the Hyperplastic Thyroid Gland With Radioactive Iodine. | 961 | ||
| Hypothyroidism | 961 | ||
| Endemic Colloid Goiter Caused by Dietary Iodide Deficiency. | 962 | ||
| Idiopathic Nontoxic Colloid Goiter. | 962 | ||
| Physiological Characteristics of Hypothyroidism. | 962 | ||
| Myxedema. | 962 | ||
| Atherosclerosis in Hypothyroidism. | 963 | ||
| Diagnostic Tests for Hypothyroidism. | 963 | ||
| Treatment of Hypothyroidism. | 963 | ||
| Cretinism | 963 | ||
| Bibliography | 963 | ||
| 78 Adrenocortical Hormones | 965 | ||
| Corticosteroids: Mineralocorticoids, Glucocorticoids, and Androgens | 965 | ||
| Synthesis and Secretion of Adrenocortical Hormones | 965 | ||
| The Adrenal Cortex Has Three Distinct Layers | 965 | ||
| Adrenocortical Hormones Are Steroids Derived from Cholesterol. | 966 | ||
| Synthetic Pathways for Adrenal Steroids. | 966 | ||
| Mineralocorticoids | 966 | ||
| Glucocorticoids | 966 | ||
| Adrenocortical Hormones Are Bound to Plasma Proteins. | 967 | ||
| Adrenocortical Hormones Are Metabolized in the Liver. | 968 | ||
| Functions of the Mineralocorticoids—Aldosterone | 968 | ||
| Mineralocorticoid Deficiency Causes Severe Renal Sodium Chloride Wasting and Hyperkalemia. | 968 | ||
| Aldosterone Is the Major Mineralocorticoid Secreted by the Adrenals. | 968 | ||
| Renal and Circulatory Effects of Aldosterone | 969 | ||
| Aldosterone Increases Renal Tubular Reabsorption of Sodium and Secretion of Potassium. | 969 | ||
| Excess Aldosterone Increases Extracellular Fluid Volume and Arterial Pressure But Has Only a Small Effect on Plasma Sodium Concentration. | 969 | ||
| Excess Aldosterone Causes Hypokalemia and Muscle Weakness; Aldosterone Deficiency Causes Hyperkalemia and Cardiac Toxicity. | 969 | ||
| Excess Aldosterone Increases Tubular Hydrogen Ion Secretion and Causes Alkalosis. | 970 | ||
| Aldosterone Stimulates Sodium and Potassium Transport in Sweat Glands, Salivary Glands, and Intestinal Epithelial Cells | 970 | ||
| Cellular Mechanism of Aldosterone Action | 970 | ||
| Possible Nongenomic Actions of Aldosterone and Other Steroid Hormones | 971 | ||
| Regulation of Aldosterone Secretion | 971 | ||
| Functions of Glucocorticoids | 972 | ||
| Effects of Cortisol on Carbohydrate Metabolism | 972 | ||
| Stimulation of Gluconeogenesis. | 972 | ||
| Decreased Glucose Utilization by Cells. | 972 | ||
| Elevated Blood Glucose Concentration and “Adrenal Diabetes.” | 973 | ||
| Effects of Cortisol on Protein Metabolism | 973 | ||
| Reduction in Cellular Protein. | 973 | ||
| Cortisol Increases Liver and Plasma Proteins. | 973 | ||
| Increased Blood Amino Acids, Diminished Transport of Amino Acids Into Extrahepatic Cells, and Enhanced Transport Into Hepatic Cells. | 973 | ||
| Effects of Cortisol on Fat Metabolism | 973 | ||
| Mobilization of Fatty Acids. | 973 | ||
| Excess Cortisol Causes Obesity. | 974 | ||
| Cortisol is Important in Resisting Stress and Inflammation | 974 | ||
| Anti-inflammatory Effects of High Levels of Cortisol | 974 | ||
| Cortisol Prevents the Development of Inflammation by Stabilizing Lysosomes and by Other Effects. | 975 | ||
| Cortisol Causes Resolution of Inflammation. | 975 | ||
| Other Effects of Cortisol | 975 | ||
| Cortisol Blocks the Inflammatory Response to Allergic Reactions. | 975 | ||
| Effect on Blood Cells and on Immunity in Infectious Diseases. | 976 | ||
| Cellular Mechanism of Cortisol Action | 976 | ||
| Regulation of Cortisol Secretion by Adrenocorticotropic Hormone from the Pituitary Gland | 976 | ||
| ACTH Stimulates Cortisol Secretion. | 976 | ||
| Chemistry of ACTH. | 976 | ||
| ACTH Secretion Is Controlled by Corticotropin-Releasing Factor From the Hypothalamus. | 976 | ||
| ACTH Activates Adrenocortical Cells to Produce Steroids by Increasing cAMP. | 976 | ||
| Physiological Stress Increases ACTH and Adrenocortical Secretion. | 976 | ||
| Inhibitory Effect of Cortisol on the Hypothalamus and on the Anterior Pituitary to Decrease ACTH Secretion. | 977 | ||
| Summary of the Cortisol Control System | 977 | ||
| Circadian Rhythm of Glucocorticoid Secretion. | 977 | ||
| Synthesis and Secretion of ACTH in Association with Melanocyte-Stimulating Hormone, Lipotropin, and Endorphin | 977 | ||
| Adrenal Androgens | 978 | ||
| Abnormalities of Adrenocortical Secretion | 979 | ||
| Hypoadrenalism (Adrenal Insufficiency)—Addison’s Disease | 979 | ||
| Mineralocorticoid Deficiency. | 979 | ||
| Glucocorticoid Deficiency. | 979 | ||
| Melanin Pigmentation. | 979 | ||
| Treatment of People with Addison’s Disease. | 979 | ||
| Addisonian Crisis. | 979 | ||
| Hyperadrenalism—Cushing’s Syndrome | 979 | ||
| Effects on Carbohydrate and Protein Metabolism | 980 | ||
| Treatment of Cushing’s Syndrome. | 980 | ||
| Primary Aldosteronism (Conn’s Syndrome) | 981 | ||
| Adrenogenital Syndrome | 981 | ||
| Bibliography | 981 | ||
| 79 Insulin, Glucagon, and Diabetes Mellitus | 983 | ||
| Physiological Anatomy of the Pancreas | 983 | ||
| Insulin and its Metabolic Effects | 983 | ||
| Insulin is a Hormone Associated with Energy Abundance | 983 | ||
| Insulin Chemistry and Synthesis | 984 | ||
| Activation of Target cell Receptors by Insulin and the Resulting Cellular Effects | 984 | ||
| Effect of Insulin on Carbohydrate Metabolism | 985 | ||
| Insulin Promotes Muscle Glucose Uptake and Metabolism | 985 | ||
| Storage of Glycogen in Muscle. | 986 | ||
| Quantitative Effect of Insulin to Facilitate Glucose Transport Through the Muscle Cell Membrane | 986 | ||
| Insulin Promotes Liver Uptake, Storage, and Use of Glucose | 986 | ||
| Glucose Is Released From the Liver Between Meals. | 986 | ||
| Insulin Promotes Conversion of Excess Glucose Into Fatty Acids and Inhibits Gluconeogenesis in the Liver. | 986 | ||
| Lack of Effect of Insulin on Glucose Uptake and Usage by the Brain | 987 | ||
| Effect of Insulin on Carbohydrate Metabolism in Other Cells | 987 | ||
| Effect Of Insulin On Fat Metabolism | 987 | ||
| Insulin Promotes Fat Synthesis and Storage | 987 | ||
| Role of Insulin in Storage of Fat in the Adipose Cells. | 987 | ||
| Insulin Deficiency Increases Use of Fat for Energy | 988 | ||
| Insulin Deficiency Causes Lipolysis of Storage Fat and Release of Free Fatty Acids. | 988 | ||
| Insulin Deficiency Increases Plasma Cholesterol and Phospholipid Concentrations. | 988 | ||
| Excess Usage of Fats During Insulin Deficiency Causes Ketosis and Acidosis. | 988 | ||
| Effect of Insulin on Protein Metabolism and Growth | 988 | ||
| Insulin Promotes Protein Synthesis and Storage | 988 | ||
| Insulin Deficiency Causes Protein Depletion and Increased Plasma Amino Acids | 989 | ||
| Insulin and Growth Hormone Interact Synergistically to Promote Growth | 989 | ||
| Mechanisms Of Insulin Secretion | 989 | ||
| Control of Insulin Secretion | 990 | ||
| Increased Blood Glucose Stimulates Insulin Secretion. | 990 | ||
| Feedback Relation Between Blood Glucose Concentration and the Insulin Secretion Rate. | 990 | ||
| Other Factors That Stimulate Insulin Secretion | 991 | ||
| Amino Acids. | 991 | ||
| Gastrointestinal Hormones. | 991 | ||
| Other Hormones and the Autonomic Nervous System. | 991 | ||
| The Role of Insulin (and Other Hormones) in “Switching” between Carbohydrate and Lipid Metabolism | 991 | ||
| Glucagon and its Functions | 992 | ||
| Effects on Glucose Metabolism | 992 | ||
| Glucagon Causes Glycogenolysis and Increased Blood Glucose Concentration | 992 | ||
| Glucagon Increases Gluconeogenesis | 992 | ||
| Other Effects of Glucagon | 992 | ||
| Regulation of Glucagon Secretion | 993 | ||
| Increased Blood Glucose Inhibits Glucagon Secretion. | 993 | ||
| Increased Blood Amino Acids Stimulate Secretion of Glucagon. | 993 | ||
| Exercise Stimulates Secretion of Glucagon. | 993 | ||
| Somatostatin Inhibits Glucagon and Insulin Secretion | 993 | ||
| Summary of Blood Glucose Regulation | 993 | ||
| Importance of Blood Glucose Regulation. | 994 | ||
| Diabetes Mellitus | 994 | ||
| Type 1 Diabetes—Deficiency of Insulin Production by Beta Cells of the Pancreas | 995 | ||
| Blood Glucose Concentration Rises to High Levels in Diabetes Mellitus. | 995 | ||
| Increased Blood Glucose Causes Loss of Glucose in the Urine. | 995 | ||
| Increased Blood Glucose Causes Dehydration. | 995 | ||
| Chronic High Glucose Concentration Causes Tissue Injury. | 995 | ||
| Diabetes Mellitus Causes Increased Utilization of Fats and Metabolic Acidosis. | 995 | ||
| Diabetes Causes Depletion of the Body’s Proteins. | 995 | ||
| Type 2 Diabetes—Resistance to the Metabolic Effects of Insulin | 996 | ||
| Obesity, Insulin Resistance, and “Metabolic Syndrome” Usually Precede the Development of Type 2 Diabetes. | 996 | ||
| Other Factors That Can Cause Insulin Resistance and Type 2 Diabetes. | 996 | ||
| Development of Type 2 Diabetes During Prolonged Insulin Resistance. | 997 | ||
| Physiology of Diagnosis of Diabetes Mellitus | 997 | ||
| Urinary Glucose. | 997 | ||
| Fasting Blood Glucose and Insulin Levels. | 997 | ||
| Glucose Tolerance Test. | 997 | ||
| Acetone Breath. | 998 | ||
| Treatment of Diabetes | 998 | ||
| Relation of Treatment to Arteriosclerosis. | 998 | ||
| Insulinoma—Hyperinsulinism | 998 | ||
| Insulin Shock and Hypoglycemia. | 998 | ||
| Bibliography | 999 | ||
| 80 Parathyroid Hormone, Calcitonin, Calcium and Phosphate Metabolism, Vitamin D, Bone, and Teeth | 1001 | ||
| Overview of Calcium and Phosphate Regulation in the Extracellular Fluid and Plasma | 1001 | ||
| Calcium in the Plasma and interstitial Fluid | 1001 | ||
| Inorganic Phosphate in the Extracellular Fluids | 1002 | ||
| Nonbone Physiological Effects of Altered Calcium and Phosphate Concentrations in the Body Fluids | 1002 | ||
| Hypocalcemia Causes Nervous System Excitement and Tetany. | 1002 | ||
| Hypercalcemia Depresses Nervous System and Muscle Activity. | 1002 | ||
| Absorption and Excretion of Calcium and Phosphate | 1002 | ||
| Intestinal Absorption and Fecal Excretion of Calcium and Phosphate. | 1002 | ||
| Renal Excretion of Calcium and Phosphate. | 1003 | ||
| Bone and Its Relation to Extracellular Calcium and Phosphate | 1003 | ||
| Organic Matrix of Bone. | 1003 | ||
| Bone Salts. | 1003 | ||
| Tensile and Compressional Strength of Bone. | 1004 | ||
| Precipitation and Absorption of Calcium and Phosphate in Bone—Equilibrium with the Extracellular Fluids | 1004 | ||
| Hydroxyapatite Does Not Precipitate in Extracellular Fluid Despite Supersaturation of Calcium and Phosphate Ions. | 1004 | ||
| Mechanism of Bone Calcification. | 1004 | ||
| Precipitation of Calcium in Nonosseous Tissues Under Abnormal Conditions. | 1004 | ||
| Calcium Exchange Between Bone and Extracellular Fluid | 1005 | ||
| Deposition and Resorption of Bone—Remodeling of Bone | 1005 | ||
| Deposition of Bone by the Osteoblasts. | 1005 | ||
| Resorption of Bone—Function of the Osteoclasts. | 1005 | ||
| Bone Deposition and Resorption Are Normally in Equilibrium. | 1006 | ||
| Value of Continual Bone Remodeling. | 1006 | ||
| Control of the Rate of Bone Deposition by Bone “Stress.” | 1006 | ||
| Repair of a Fracture Activates Osteoblasts. | 1007 | ||
| Vitamin D | 1007 | ||
| Cholecalciferol (Vitamin D3) Is Formed in the Skin. | 1007 | ||
| Cholecalciferol Is Converted to 25-Hydroxycholecalciferol in the Liver. | 1007 | ||
| Formation of 1,25-Dihydroxycholecalciferol in the Kidneys and Its Control by Parathyroid Hormone. | 1007 | ||
| Calcium Ion Concentration Controls the Formation of 1,25-Dihydroxycholecalciferol. | 1008 | ||
| Actions of Vitamin D | 1008 | ||
| “Hormonal” Effect of Vitamin D to Promote Intestinal Calcium Absorption. | 1008 | ||
| Vitamin D Promotes Phosphate Absorption by the Intestines. | 1009 | ||
| Vitamin D Decreases Renal Calcium and Phosphate Excretion. | 1009 | ||
| Effect of Vitamin D on Bone and Its Relation to Parathyroid Hormone Activity. | 1009 | ||
| Parathyroid Hormone | 1009 | ||
| Physiological Anatomy of the Parathyroid Glands. | 1009 | ||
| Chemistry of Parathyroid Hormone. | 1009 | ||
| Effect of Parathyroid Hormone On Calcium and Phosphate Concentrations in the Extracellular Fluid | 1010 | ||
| Parathyroid Hormone Mobilizes Calcium and Phosphate From the Bone | 1010 | ||
| Rapid Phase of Calcium and Phosphate Mobilization From Bone—Osteolysis. | 1010 | ||
| Slow Phase of Bone Resorption and Calcium Phosphate Release—Activation of the Osteoclasts. | 1011 | ||
| Parathyroid Hormone Decreases Calcium Excretion and Increases Phosphate Excretion by the Kidneys | 1011 | ||
| Parathyroid Hormone Increases Intestinal Absorption of Calcium and Phosphate | 1011 | ||
| Cyclic Adenosine Monophosphate Mediates the Effects of Parathyroid Hormone. | 1011 | ||
| Control of Parathyroid Secretion by Calcium Ion Concentration | 1011 | ||
| Summary of Effects of Parathyroid Hormone | 1012 | ||
| Calcitonin | 1012 | ||
| Increased Plasma Calcium Concentration Stimulates Calcitonin Secretion. | 1012 | ||
| Calcitonin Decreases Plasma Calcium Concentration. | 1013 | ||
| Calcitonin Has a Weak Effect on Plasma Calcium Concentration in Adult Humans. | 1013 | ||
| Summary of Control of Calcium Ion Concentration | 1013 | ||
| Buffer Function of the Exchangeable Calcium in Bones—The First Line of Defense. | 1013 | ||
| Hormonal Control of Calcium Ion Concentration—The Second Line of Defense. | 1013 | ||
| Pathophysiology of Parathyroid Hormone, Vitamin D, and Bone Disease | 1014 | ||
| Hypoparathyroidism | 1014 | ||
| Treatment of Hypoparathyroidism with PTH and Vitamin D. | 1014 | ||
| Primary Hyperparathyroidism | 1014 | ||
| Bone Disease in Hyperparathyroidism. | 1014 | ||
| Effects of Hypercalcemia in Hyperparathyroidism. | 1014 | ||
| Parathyroid Poisoning and Metastatic Calcification. | 1015 | ||
| Formation of Kidney Stones in Hyperparathyroidism. | 1015 | ||
| Secondary Hyperparathyroidism | 1015 | ||
| Rickets Caused by Vitamin D Deficiency | 1015 | ||
| Plasma Concentrations of Calcium and Phosphate Decrease in Rickets. | 1015 | ||
| Rickets Weakens the Bones. | 1015 | ||
| Tetany in Rickets. | 1015 | ||
| Treatment of Rickets. | 1015 | ||
| Osteomalacia—“Adult Rickets.” | 1015 | ||
| Osteomalacia and Rickets Caused by Renal Disease. | 1016 | ||
| Osteoporosis—Decreased Bone Matrix | 1016 | ||
| Physiology of the Teeth | 1016 | ||
| Function of the Different Parts of the Teeth | 1016 | ||
| Enamel. | 1016 | ||
| Dentin. | 1016 | ||
| Cementum. | 1017 | ||
| Pulp. | 1017 | ||
| Dentition. | 1017 | ||
| Formation of the Teeth. | 1017 | ||
| Eruption of Teeth. | 1017 | ||
| Development of the Permanent Teeth. | 1017 | ||
| Metabolic Factors Influence Development of the Teeth. | 1017 | ||
| Mineral Exchange in Teeth. | 1018 | ||
| Dental Abnormalities | 1018 | ||
| Caries and the Role of Bacteria and Ingested Carbohydrates. | 1018 | ||
| Role of Fluorine in Preventing Caries. | 1018 | ||
| Malocclusion. | 1018 | ||
| Bibliography | 1018 | ||
| 81 Reproductive and Hormonal Functions of the Male (and Function of the Pineal Gland) | 1021 | ||
| Physiological Anatomy of the Male Sexual Organs | 1021 | ||
| Spermatogenesis | 1021 | ||
| Steps of Spermatogenesis | 1021 | ||
| Meiosis. | 1022 | ||
| Sex Chromosomes. | 1022 | ||
| Formation of Sperm. | 1023 | ||
| Hormonal Factors That Stimulate Spermatogenesis | 1023 | ||
| Maturation of Sperm in the Epididymis | 1023 | ||
| Storage of Sperm in the Testes. | 1023 | ||
| Physiology of the Mature Sperm. | 1024 | ||
| Function of the Seminal Vesicles | 1024 | ||
| Function of the Prostate Gland | 1024 | ||
| Semen | 1024 | ||
| “Capacitation” of Spermatozoa Is Required for Fertilization of the Ovum | 1024 | ||
| Acrosome Enzymes, the “Acrosome Reaction,” and Penetration of the Ovum | 1025 | ||
| Why Does Only One Sperm Enter the Oocyte? | 1025 | ||
| Abnormal Spermatogenesis and Male Fertility | 1025 | ||
| Effect of Temperature on Spermatogenesis. | 1025 | ||
| Cryptorchidism. | 1026 | ||
| Effect of Sperm Count on Fertility. | 1026 | ||
| Effect of Sperm Morphology and Motility on Fertility. | 1026 | ||
| Male Sexual Act | 1026 | ||
| Neuronal Stimulus for Performance of the Male Sexual Act | 1026 | ||
| Psychic Element of Male Sexual Stimulation. | 1026 | ||
| Integration of the Male Sexual Act in the Spinal Cord. | 1027 | ||
| Stages of the Male Sexual Act | 1027 | ||
| Penile Erection—Role of the Parasympathetic Nerves. | 1027 | ||
| Lubrication Is a Parasympathetic Function. | 1027 | ||
| Emission and Ejaculation Are Functions of the Sympathetic Nerves. | 1027 | ||
| Testosterone and Other Male Sex Hormones | 1028 | ||
| Secretion, Metabolism, and Chemistry of the Male Sex Hormone | 1028 | ||
| Secretion of Testosterone by the Interstitial Cells of Leydig in the Testes. | 1028 | ||
| Secretion of Androgens Elsewhere in the Body. | 1028 | ||
| Chemistry of the Androgens. | 1028 | ||
| Metabolism of Testosterone. | 1028 | ||
| Degradation and Excretion of Testosterone. | 1028 | ||
| Production of Estrogen in the Male. | 1028 | ||
| Functions of Testosterone | 1029 | ||
| Functions of Testosterone During Fetal Development | 1029 | ||
| Effect of Testosterone to Cause Descent of the Testes. | 1029 | ||
| Effect of Testosterone on Development of Adult Primary and Secondary Sexual Characteristics | 1030 | ||
| Effect on the Distribution of Body Hair. | 1030 | ||
| Male Pattern Baldness. | 1030 | ||
| Effect on the Voice. | 1030 | ||
| Testosterone Increases Thickness of the Skin and Can Contribute to the Development of Acne. | 1030 | ||
| Testosterone Increases Protein Formation and Muscle Development. | 1030 | ||
| Testosterone Increases Bone Matrix and Causes Calcium Retention. | 1030 | ||
| Testosterone Increases the Basal Metabolic Rate. | 1030 | ||
| Testosterone Increases Red Blood Cells. | 1031 | ||
| Effect on Electrolyte and Water Balance. | 1031 | ||
| Basic Intracellular Mechanism of Action of Testosterone | 1031 | ||
| Control of Male Sexual Functions by Hormones from the Hypothalamus and Anterior Pituitary Gland | 1031 | ||
| GnRH and Its Effect in Increasing the Secretion of Luteinizing Hormone and Follicle-Stimulating Hormone | 1031 | ||
| Gonadotropic Hormones: Luteinizing Hormone and Follicle-Stimulating Hormone | 1031 | ||
| Regulation of Testosterone Production by Luteinizing Hormone. | 1032 | ||
| Inhibition of Anterior Pituitary Secretion of LH and FSH by Testosterone-Negative Feedback Control of Testosterone Secretion. | 1032 | ||
| Regulation of Spermatogenesis by Follicle-Stimulating Hormone and Testosterone | 1032 | ||
| Role of Inhibin in Negative Feedback Control of Seminiferous Tubule Activity. | 1032 | ||
| Human Chorionic Gonadotropin Secreted by the Placenta During Pregnancy Stimulates Testosterone Secretion by the Fetal Testes | 1033 | ||
| Puberty and Regulation of Its Onset | 1033 | ||
| Male Adult Sexual Life and Male Climacteric. | 1033 | ||
| Abnormalities of Male Sexual Function | 1033 | ||
| The Prostate Gland and Its Abnormalities | 1033 | ||
| Hypogonadism in the Male | 1033 | ||
| Testicular Tumors and Hypergonadism in the Male | 1034 | ||
| Erectile Dysfunction in the Male | 1034 | ||
| The Function of the Pineal Gland in Controlling Seasonal Fertility in Some Animals | 1034 | ||
| Bibliography | 1035 | ||
| 82 Female Physiology Before Pregnancy and Female Hormones | 1037 | ||
| Physiological Anatomy of the Female Sexual Organs | 1037 | ||
| Oogenesis and Follicular Development in the Ovaries | 1037 | ||
| Female Hormonal System | 1039 | ||
| Monthly Ovarian Cycle; Function of the Gonadotropic Hormones | 1039 | ||
| Gonadotropic Hormones and Their Effects on the Ovaries | 1039 | ||
| Ovarian Follicle Growth—The Follicular Phase of the Ovarian Cycle | 1040 | ||
| Development of Antral and Vesicular Follicles. | 1040 | ||
| Only One Follicle Fully Matures Each Month, and the Remainder Undergo Atresia. | 1041 | ||
| Ovulation | 1041 | ||
| A Surge of Luteinizing Hormone Is Necessary for Ovulation. | 1041 | ||
| Initiation of Ovulation. | 1041 | ||
| Corpus Luteum—The Luteal Phase of the Ovarian Cycle | 1042 | ||
| Luteinizing Function of Luteinizing Hormone. | 1042 | ||
| Secretion by the Corpus Luteum: An Additional Function of Luteinizing Hormone. | 1042 | ||
| Involution of the Corpus Luteum and Onset of the Next Ovarian Cycle. | 1042 | ||
| Summary | 1042 | ||
| Functions of the Ovarian Hormones—Estradiol and Progesterone | 1042 | ||
| Chemistry of the Sex Hormones | 1043 | ||
| Estrogens. | 1043 | ||
| Progestins. | 1043 | ||
| Synthesis of the Estrogens and Progestins. | 1043 | ||
| Estrogens and Progesterone Are Transported in the Blood Bound to Plasma Proteins. | 1044 | ||
| Functions of the Liver in Estrogen Degradation. | 1044 | ||
| Fate of Progesterone. | 1044 | ||
| Functions of the Estrogens— Their Effects on the Primary and Secondary Female Sex Characteristics | 1044 | ||
| Effect of Estrogens on the Uterus and External Female Sex Organs. | 1044 | ||
| Effect of Estrogens on the Fallopian Tubes. | 1045 | ||
| Effect of Estrogens on the Breasts. | 1045 | ||
| Effect of Estrogens on the Skeleton. | 1045 | ||
| Osteoporosis of the Bones Caused by Estrogen Deficiency in Old Age. | 1045 | ||
| Estrogens Slightly Increase Protein Deposition. | 1045 | ||
| Estrogens Increase Body Metabolism and Fat Deposition. | 1045 | ||
| Estrogens Have Little Effect on Hair Distribution. | 1045 | ||
| Effect of Estrogens on the Skin. | 1046 | ||
| Effect of Estrogens on Electrolyte Balance. | 1046 | ||
| Functions of Progesterone | 1046 | ||
| Progesterone Promotes Secretory Changes in the Uterus. | 1046 | ||
| Effect of Progesterone on the Fallopian Tubes. | 1046 | ||
| Progesterone Promotes Development of the Breasts. | 1046 | ||
| Monthly Endometrial Cycle and Menstruation | 1046 | ||
| Proliferative Phase (Estrogen Phase) of the Endometrial Cycle, Occurring Before Ovulation. | 1046 | ||
| Secretory Phase (Progestational Phase) of the Endometrial Cycle, Occurring After Ovulation. | 1046 | ||
| Menstruation. | 1047 | ||
| Leukorrhea During Menstruation. | 1047 | ||
| Regulation of the Female Monthly Rhythm—Interplay Between the Ovarian and Hypothalamic-Pituitary Hormones | 1047 | ||
| The Hypothalamus Secretes GnRH, Which Causes the Anterior Pituitary Gland to Secrete LH and FSH | 1047 | ||
| Intermittent, Pulsatile Secretion of GnRH by the Hypothalamus Stimulates Pulsatile Release of LH from the Anterior Pituitary Gland. | 1047 | ||
| Hypothalamic Centers for Release of Gonadotropin-Releasing Hormone. | 1048 | ||
| Negative Feedback Effects of Estrogen and Progesterone to Decrease LH and FSH Secretion | 1048 | ||
| Inhibin from the Corpus Luteum Inhibits FSH and LH Secretion. | 1048 | ||
| Positive Feedback Effect of Estrogen Before Ovulation—The Preovulatory Luteinizing Hormone Surge | 1048 | ||
| Feedback Oscillation of the Hypothalamic-Pituitary- Ovarian System | 1049 | ||
| Anovulatory Cycles—Sexual Cycles at Puberty | 1050 | ||
| Puberty and Menarche | 1050 | ||
| Menopause | 1050 | ||
| Abnormalities of Secretion by the Ovaries | 1051 | ||
| Hypogonadism-Reduced Secretion by the Ovaries. | 1051 | ||
| Irregularity of Menses, and Amenorrhea Caused by Hypogonadism. | 1051 | ||
| Hypersecretion by the Ovaries. | 1051 | ||
| Female Sexual Act | 1051 | ||
| Stimulation of the Female Sexual Act. | 1051 | ||
| Female Erection and Lubrication. | 1052 | ||
| Female Orgasm. | 1052 | ||
| Female Fertility | 1052 | ||
| Fertile Period of Each Sexual Cycle. | 1052 | ||
| Rhythm Method of Contraception. | 1052 | ||
| Hormonal Suppression of Fertility—“The Pill” | 1053 | ||
| Abnormal Conditions That Cause Female Sterility | 1053 | ||
| Bibliography | 1054 | ||
| 83 Pregnancy and Lactation | 1055 | ||
| Maturation and Fertilization of the Ovum | 1055 | ||
| Entry of the Ovum Into the Fallopian Tube (Uterine Tube). | 1055 | ||
| Fertilization of the Ovum. | 1055 | ||
| What Determines the Sex of the Fetus that is Created? | 1055 | ||
| Transport of the Fertilized Ovum in the Fallopian Tube | 1056 | ||
| Implantation of the Blastocyst in the Uterus | 1056 | ||
| Early Nutrition of the Embryo | 1057 | ||
| Anatomy and Function of the Placenta | 1057 | ||
| Placental Permeability and Membrane Diffusion Conductance | 1057 | ||
| Diffusion of Oxygen Through the Placental Membrane. | 1058 | ||
| Diffusion of Carbon Dioxide Through the Placental Membrane. | 1059 | ||
| Diffusion of Foodstuffs Through the Placental Membrane. | 1059 | ||
| Excretion of Waste Products Through the Placental Membrane. | 1059 | ||
| Hormonal Factors in Pregnancy | 1059 | ||
| Human Chorionic Gonadotropin Causes Persistence of the Corpus Luteum and Prevents Menstruation | 1059 | ||
| Function of Human Chorionic Gonadotropin. | 1059 | ||
| Human Chorionic Gonadotropin Stimulates the Male Fetal Testes to Produce Testosterone. | 1060 | ||
| Secretion of Estrogens by the Placenta | 1060 | ||
| Function of Estrogen in Pregnancy. | 1060 | ||
| Secretion of Progesterone by the Placenta | 1061 | ||
| Human Chorionic Somatomammotropin | 1061 | ||
| Other Hormonal Factors in Pregnancy | 1061 | ||
| Pituitary Secretion. | 1061 | ||
| Increased Corticosteroid Secretion. | 1061 | ||
| Increased Thyroid Gland Secretion. | 1061 | ||
| Increased Parathyroid Gland Secretion. | 1061 | ||
| Secretion of “Relaxin” by the Ovaries and Placenta. | 1062 | ||
| Response of the Mother’s Body to Pregnancy | 1062 | ||
| Weight Gain in the Pregnant Woman | 1062 | ||
| Metabolism During Pregnancy | 1062 | ||
| Nutrition During Pregnancy | 1062 | ||
| Changes in the Maternal Circulatory System During Pregnancy | 1062 | ||
| Blood Flow Through the Placenta and Maternal Cardiac Output Increase During Pregnancy. | 1062 | ||
| Maternal Blood Volume Increases During Pregnancy. | 1062 | ||
| Maternal Respiration Increases During Pregnancy. | 1063 | ||
| Maternal Kidney Function During Pregnancy | 1063 | ||
| Amniotic Fluid and Its Formation | 1063 | ||
| Preeclampsia and Eclampsia | 1063 | ||
| Parturition | 1064 | ||
| Increased Uterine Excitability Near Term | 1064 | ||
| Hormonal Factors That Increase Uterine Contractility | 1064 | ||
| Increased Ratio of Estrogens to Progesterone. | 1064 | ||
| Oxytocin Causes Contraction of the Uterus. | 1064 | ||
| Effect of Fetal Hormones on the Uterus. | 1064 | ||
| Mechanical Factors That Increase Uterine Contractility | 1064 | ||
| Stretch of the Uterine Musculature. | 1064 | ||
| Stretch or Irritation of the Cervix. | 1064 | ||
| Onset of Labor—A Positive Feedback Mechanism for its Initiation | 1065 | ||
| Abdominal Muscle Contractions During Labor | 1065 | ||
| Mechanics of Parturition | 1065 | ||
| Separation and Delivery of the Placenta | 1066 | ||
| Labor Pains | 1066 | ||
| Involution of the Uterus After Parturition | 1066 | ||
| Lactation | 1066 | ||
| Development of the Breasts | 1066 | ||
| Estrogens Stimulate Growth of the Ductal System of the Breasts. | 1066 | ||
| Progesterone Is Required for Full Development of the Lobule-Alveolar System. | 1066 | ||
| Prolactin Promotes Lactation | 1067 | ||
| The Hypothalamus Secretes Prolactin Inhibitory Hormone. | 1068 | ||
| Suppression of the Female Ovarian Cycles in Nursing Mothers for Many Months After Delivery. | 1068 | ||
| Ejection (or “Let-Down”) Process in Milk Secretion—Function of Oxytocin | 1068 | ||
| Inhibition of Milk Ejection. | 1068 | ||
| Milk Composition and the Metabolic Drain on the Mother Caused By Lactation | 1068 | ||
| Antibodies and Other Anti-infectious Agents in Milk. | 1069 | ||
| Bibliography | 1069 | ||
| 84 Fetal and Neonatal Physiology | 1071 | ||
| Growth and Functional Development of the Fetus | 1071 | ||
| Development of the Organ Systems | 1071 | ||
| Circulatory System. | 1071 | ||
| Formation of Blood Cells. | 1071 | ||
| Respiratory System. | 1071 | ||
| Nervous System. | 1072 | ||
| Gastrointestinal Tract. | 1072 | ||
| Kidneys. | 1072 | ||
| Fetal Metabolism | 1072 | ||
| Metabolism of Calcium and Phosphate | 1072 | ||
| Accumulation of Iron | 1072 | ||
| Utilization and Storage of Vitamins | 1072 | ||
| Adjustments of the Infant to Extrauterine Life | 1073 | ||
| Onset of Breathing | 1073 | ||
| Cause of Breathing at Birth. | 1073 | ||
| Delayed or Abnormal Breathing at Birth—Danger of Hypoxia. | 1073 | ||
| Degree of Hypoxia That an Infant Can Tolerate. | 1073 | ||
| Expansion of the Lungs at Birth. | 1073 | ||
| Respiratory Distress Syndrome Is Caused When Surfactant Secretion Is Deficient. | 1073 | ||
| Circulatory Readjustments at Birth | 1074 | ||
| Specific Anatomical Structure of the Fetal Circulation | 1074 | ||
| Changes in Fetal Circulation at Birth | 1075 | ||
| Decreased Pulmonary and Increased Systemic Vascular Resistances at Birth. | 1075 | ||
| Closure of the Foramen Ovale. | 1075 | ||
| Closure of the Ductus Arteriosus. | 1075 | ||
| Closure of the Ductus Venosus. | 1075 | ||
| Nutrition of the Neonate | 1076 | ||
| Special Functional Problems in the Neonate | 1076 | ||
| Respiratory System | 1076 | ||
| Circulation | 1076 | ||
| Blood Volume. | 1076 | ||
| Cardiac Output. | 1076 | ||
| Arterial Pressure. | 1076 | ||
| Blood Characteristics. | 1076 | ||
| Neonatal Jaundice and Erythroblastosis Fetalis. | 1077 | ||
| Fluid Balance, Acid-Base Balance, and Renal Function | 1077 | ||
| Liver Function | 1077 | ||
| Digestion, Absorption, and Metabolism of Energy Foods and Nutrition | 1077 | ||
| Increased Metabolic Rate and Poor Body Temperature Regulation. | 1077 | ||
| Nutritional Needs During the Early Weeks of Life. | 1077 | ||
| Need for Calcium and Vitamin D. | 1078 | ||
| Necessity for Iron in the Diet. | 1078 | ||
| Vitamin C Deficiency in Infants. | 1078 | ||
| Immunity | 1078 | ||
| Allergy. | 1078 | ||
| Endocrine Problems | 1078 | ||
| Special Problems of Prematurity | 1079 | ||
| Immature Development of the Premature Infant | 1079 | ||
| Respiration. | 1079 | ||
| Gastrointestinal Function. | 1079 | ||
| Function of Other Organs. | 1079 | ||
| Instability of the Homeostatic Control Systems in Premature Infants | 1079 | ||
| Instability of Body Temperature. | 1079 | ||
| Danger of Blindness Caused by Excess Oxygen Therapy in the Premature Infant | 1079 | ||
| Growth and Development of the Child | 1080 | ||
| Behavioral Growth | 1080 | ||
| Bibliography | 1080 | ||
| Unit XV Sports Physiology | 1083 | ||
| 85 Sports Physiology | 1085 | ||
| Female and Male Athletes | 1085 | ||
| Muscles in Exercise | 1085 | ||
| Strength, Power, and Endurance of Muscles | 1085 | ||
| Muscle Metabolic Systems in Exercise | 1086 | ||
| Adenosine Triphosphate. | 1086 | ||
| Phosphocreatine-Creatine System | 1087 | ||
| Glycogen–Lactic Acid System. | 1087 | ||
| Aerobic System. | 1087 | ||
| What Types of Sports Use Which Energy Systems? | 1087 | ||
| Recovery of the Muscle Metabolic Systems After Exercise. | 1088 | ||
| Recovery of the Aerobic System After Exercise. | 1088 | ||
| Oxygen Debt. | 1088 | ||
| Recovery of Muscle Glycogen. | 1088 | ||
| Nutrients Used During Muscle Activity | 1089 | ||
| Effect of Athletic Training on Muscles and Muscle Performance | 1089 | ||
| Importance of Maximal Resistance Training. | 1089 | ||
| Muscle Hypertrophy. | 1090 | ||
| Fast-Twitch and Slow-Twitch Muscle Fibers. | 1090 | ||
| Hereditary Differences Among Athletes for Fast-Twitch Versus Slow-Twitch Muscle Fibers. | 1090 | ||
| Respiration in Exercise | 1090 | ||
| Oxygen Consumption and Pulmonary Ventilation in Exercise. | 1090 | ||
| Limits of Pulmonary Ventilation. | 1090 | ||
| Effect of Training on max. | 1091 | ||
| Oxygen-Diffusing Capacity of Athletes. | 1091 | ||
| Blood Gases During Exercise. | 1091 | ||
| Effect of Smoking on Pulmonary Ventilation in Exercise. | 1092 | ||
| Cardiovascular System in Exercise | 1092 | ||
| Muscle Blood Flow. | 1092 | ||
| Work Output, Oxygen Consumption, and Cardiac Output During Exercise. | 1092 | ||
| Effect of Training on Heart Hypertrophy and on Cardiac Output. | 1093 | ||
| Role of Stroke Volume and Heart Rate in Increasing the Cardiac Output. | 1093 | ||
| Relation of Cardiovascular Performance to max. | 1093 | ||
| Effect of Heart Disease and Old Age on Athletic Performance. | 1094 | ||
| Body Heat in Exercise | 1094 | ||
| Heatstroke. | 1094 | ||
| Body Fluids and Salt in Exercise | 1094 | ||
| Replacement of Sodium Chloride and Potassium. | 1094 | ||
| Drugs and Athletes | 1095 | ||
| Body Fitness Prolongs Life | 1095 | ||
| Bibliography | 1095 | ||
| Index | 1097 | ||
| A | 1097 | ||
| B | 1102 | ||
| C | 1105 | ||
| D | 1110 | ||
| E | 1111 | ||
| F | 1114 | ||
| G | 1116 | ||
| H | 1118 | ||
| I | 1121 | ||
| J | 1122 | ||
| K | 1122 | ||
| L | 1123 | ||
| M | 1124 | ||
| N | 1127 | ||
| O | 1128 | ||
| P | 1129 | ||
| Q | 1134 | ||
| R | 1134 | ||
| S | 1136 | ||
| T | 1141 | ||
| U | 1143 | ||
| V | 1143 | ||
| W | 1145 | ||
| X | 1145 | ||
| Y | 1145 | ||
| Z | 1145 | ||
| IBC_Common Lab Measurements | IBC1 |