Cardiac Protection by Halothane Following Ischemia and Calcium Paradox
Calcium ions play a crucial role in the regulation of cardiac function and their movements may be profoundly affected in various pathophysiological conditions. Specifically, reper fusion of the severely ischemic myocardium is associated with a rapid net gain in intracellular calcium, largely in the mitochondria, and the development of contraction band necrosis (Shen and Jennings, 1972, Nayleret al., 1985). The extent of calcium accumulation on reperfusion of the ischemic heart is related to the severity and duration of ischemia and the degree of mechanical recovery (Henryet al., 1977; Bourdillon and Poole-Wilson, 1981). A marked calcium accumulation is also produced by exposure to calcium-containing solutions following a brief period of exposure to calcium-free perfusate, a phenomenon known as the “calcium paradox” (Ruigroket al., 1985). While the mechanisms underlying myocardial injury under these conditions are controversial, several interventions limiting depletion of high-energy phosphate stores and calcium accumulation have been shown to have a protective effect on the heart (Bourdillon and Poole-Wilson, 1982). Pretreatment with calcium-blocking agents before calcium-free perfusion or the onset of ischemia is reported to reduce the degree of ultrastructural damage and enhance recovery of contractile function (Wattset al., 1980; Ohharaet al., 1982). This potential beneficial intervention may have relevance to the clinical problems of reducing cardiac injury and restoring ventricular function following transient ischemic episodes and the use of cardioplegic solutions in patients undergoing myocardial revascularization.
KeywordsToxicity Magnesium Depression Ischemia Superoxide
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