Effects of Volatile Anesthetics on the Intracellular Calcium Transient and Calcium Current in Cardiac Muscle Cells
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Volatile anesthetics at clinically useful concentrations depress the contractile force of the heart, and this effect in part contributes to a significant decrement of cardiovascular homeostasis. The mechanism of action underlying the negative inotropic effect of volatile anesthetics is not fully understood. There are several mechanisms by which agents may directly alter contractile performance of cardiac muscle. The first group represents the “upstream” mechanisms whereby intracellular calcium transients are mostly influenced by a variety of effectors at the surface membrane and sarcoplasmic reticulum. In addition, changes in sensitivity of troponin-C to calcium, and an altered response of the myofilaments to a given level of occupancy of the calcium binding sites on troponin C (“downstream” mechanisms) need to be considered as well. Accumulating evidence suggests that volatile anesthetics have multiple actions relevant to cardiac contractility, including a decrease in the sarcolemmal flux of calcium, a change in SR function, and a decrease in the level of intracellular ionized calcium during systole as well as a modification in the responsiveness of the contractile proteins to activation by calcium. A variety of the newest technology and methods, including the measurements of inward calcium current (ICa), measurement of calcium transients, and myofibrillar responsiveness to calcium, were utilized in the studies reported here in order to improve our knowledge of the effects of volatile anesthetics on cardiac muscle.
KeywordsPapillary Muscle Anesthetic Agent Calcium Current Contractile Force Volatile Anesthetic
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