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Although ischemia-reperfusion (I/R) has been shown to affect subcellular organelles that regulate the intracellular Ca2+ concentration (Ca2+i), very little information regarding the Ca2+ handling ability of cardiomyocytes obtained from I/R hearts is available. To investigate changes in Ca2+i due to I/R, rat hearts in vitro were subjected to 10-30 min of ischemia followed by 5-30 min of reperfusion. Cardiomyocytes from these hearts were isolated and purified; Ca2+i was measured by employing fura-2 microfluorometry. Reperfusion for 30 min of the 20-min ischemic hearts showed attenuated cardiac performance, whereas basal Ca2+i as well as the KCl-induced increase in Ca2+i and isoproterenol (Iso)-induced increase in Ca2+i in cardiomyocytes remained unaltered. On the other hand, reperfusion of the 30-min ischemic hearts for different periods revealed marked changes in cardiac function, basal Ca2+i, and Iso-induced increase in Ca2+i without any alterations in the KCl-induced increase in Ca2+i or S(-)-BAY K 8644-induced increase in Ca2+i. The I/R-induced alterations in cardiac function, basal Ca2+i, and Iso-induced increase in Ca2+i in cardiomyocytes were attenuated by an antioxidant mixture containing superoxide dismutase and catalase as well as by ischemic preconditioning. The observed changes due to I/R were simulated in hearts perfused with H2O2 for 30 min. These results suggest that abnormalities in basal Ca2+i as well as mobilization of Ca2+i upon beta-adrenoceptor stimulation in cardiomyocytes are dependent on the duration of ischemic injury to the myocardium. Furthermore, Ca2+ handling defects in cardiomyocytes appear to be mediated through oxidative stress in I/R hearts.
Saini et al. (2005) studied this question.
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