Energy Production and Utilization in Contractile Failure Due to Intracellular Calcium Overload
Intracellular calcium overload has been suggested to cause myocardial cell damage and contractile failure (6, 7, 10); however, the mechanisms of the calcium-induced pathophysiologic changes are poorly understood. Recently, intracellular calcium overload has been demonstrated to occur upon reperfusing rat hearts following a few minutes of perfusion with Ca2+-free medium (1). Reperfusion of the Ca2+-deprived hearts with a normal medium failed to restore their ability to generate contractile force and caused a further deterioration of cardiac ultrastructure (12, 22, 26, 27). Furthermore, dramatic alterations in the abilities of mitochondrial and sarcoplasmic reticular (microsomal) fractions to transport calcium have been observed upon reperfusing the Ca2+ -deprived hearts (2, 13). Although high energy phosphate stores, creatine phosphate (CrP) and ATP, have been found to be depressed in reperfused hearts (.3, 4, 5, 14, 20, 21), the exact reason for these metabolic changes is not clear at present.
KeywordsATPase Activity Free Medium Normal Medium Control Heart Calcium Paradox
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