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Key Concepts

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  • Membrane potentials are created by energy-dependent ion pumps that segregate charged ions on either side of hydrophobic cell membrane.

  • Cell depolarization is possible because channels open within the hydrophobic membrane to allow charged ions, driven by concentration gradients, to cross the membrane.

  • Trigger for the opening of transmembrane ion channel is typically a change in the membrane potential. Different channels are triggered to open at different membrane potentials.

  • The sarcomere is the contractile element of the myocyte. Each sarcomere is composed of a series of parallel myofilaments. Coaxial movement of these myofilaments, some of which are tethered to the ends of the sarcomere, result in sarcomere shortening.

  • The strength of contraction is influenced by resting length of the myocyte, sudden stretch of the myocyte, or rapidly repeated contraction of the myocyte. Speed of shortening is influenced by afterload.

  • A ventricle exposed chronically to high afterload will adapt by concentric hypertrophy because this reduces wall stress according to Laplace's law.

  • Myocardium receiving insufficient energy supply will die (infarction), become dysfunctional (ischemia), or reduce its energy needs (hibernate). Reperfused tissue is termed “stunned” if it does not contract up to its potential in spite of adequate energy supply.

  • Diastole is more energy demanding than systole, and diastolic dysfunction can be more difficult to treat than systolic dysfunction.

  • Dysfunctional endothelium leads to vascular occlusion by (1) exposing underlying tissue factor to circulating factor VII, initiating thrombosis, (2) not allowing for the interaction of thrombin with thrombomodulin and the subsequent activation of protein C to its anticoagulant form, (3) not producing nitric oxide, which is important to help decrease platelet activation, decrease vasospasm, and decrease vascular inflammation.

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Basic Myocyte Physiology

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Physiology of the Myocyte Cell Membrane
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The human body is composed predominantly of salts and water. This pool of salts and water is segregated into functional units (cells and their intracellular components) that locally alter the concentration of the salts they contain. Hydrophobic phospholipid membranes surrounding the cells (and intracellular compartments) regulate the exit/entrance of water-soluble salts and allow the cells to maintain this individualized environment (Fig. 23-1).1 Units within these phospholipid membranes actively adjust the ion content within the cell (or intracellular compartment). For example, an energy-dependent sodium (Na+), potassium (K+) pump extrudes Na+ ions from the cell and takes K+ ions into the cell at an exchange of three Na+ ions extruded per two K+ ions taken in. This allows cells to raise intracellular K+ concentrations and lower intracellular Na+. Another pump extrudes calcium (Ca2+) in exchange for Na+. This decreases Ca2+ concentrations in the intracellular (compared with the extracellular) fluid, but allows Na+ to reenter the cell. This pump is driven by the Na+ gradient created by the energy-dependent Na+, K+ pump. Other channels within the membrane ...

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