Abstract
Perfusion of all mammalian heart muscle except hamster with Ca2+-free Tyrode and thereafter reperfusion with normal Tyrode causes irreversible damage, the calcium paradox. Our study aims at deciphering the role of creatine kinase, high energy phosphates and Ca2+influx in the genesis of myocardial injury in the rat and comparing it with the hamster. Isolated hearts from hamster and rats were perfused in the Langendorff mode at 37°C for 30 min with normal Tyrode, for 15 min with Ca2+-free Tyrode and thereafter for 30 min of reperfusion with normal Tyrode. The `high energy phosphate compound' levels were monitored by31P-NMR, creatine kinase (CK) release was measured in the perfusate.45Ca influx was estimated in the papillary muscle. We observed that in the rat heart: (a) high energy phosphate levels declined significantly within 1 min of Ca2+reperfusion; (b) a massive release of CK occurred upon Ca2+reperfusion; (c) there was a significant increase of Ca2+influx. In the hamster heart, there was preservation of high energy phosphates, CK release was prevented completely and no rise in45Ca influx was observed upon Ca2+reperfusion. These results suggest that the hamster heart has a remarkable capacity for Ca2+homeostasis which protects the heart from Ca2+overload. 2000 Academic Press@p$hr
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