Abstract
Calcium (Ca 2+) overload is an important pathophysiological factor in myocardial ischemic/reperfusion injury. We investigated the effects of a cardioprotective drug, MCC-135, 5-methyl-2-(1-piperazinyl) benzenesulfonic acid monohydrate, on (1) cardiac contractile dysfunction and Ca 2+ overload induced by ischemia and reperfusion, and (2) the Na +/Ca 2+ exchanger in Langendorff-perfused rat hearts. Low-flow 45-min ischemia and 30-min reperfusion decreased developed tension and increased ventricular Ca 2+ content, effects which were ameliorated by MCC-135 and amiloride given after reperfusion. Combination of intracellular Na + overload induced by monensin (Na + ionophore; 5 μM) and zero-flow 15-min ischemia followed by 30-min reperfusion resulted in a decrease in developed tension and in the intracellular Na +-dependent increase in ventricular Ca 2+ content. MCC-135 and the highest dose of amiloride given after reperfusion reduced the increase in ventricular Ca 2+ content, whereas developed tension was increased only with MCC-135. These results suggest that the cardioprotective effect of MCC-135 in ischemia/reperfusion is associated with suppression of Ca 2+ overload and is attributable to inhibition of intracellular Na +-dependent Ca 2+ influx via the Na +/Ca 2+ exchanger.
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