The hamster heart: A paradox in itself

Perfusion of all mammalian heart muscle except hamster with Ca2+-free Tyrod e and thereafter reperfusion with normal Tyrode causes irreversible damage, the calcium paradox. Our study aims at deciphering the role of creatine ki nase, high energy phosphates and Ca2+ influx in the genesis of myocardial i njury in the:rat and comparing it with the hamster. Isolated hearts from ha mster and rats were perfused in the Langendorff mode at 37 degrees C for 30 min with normal Tyrode, for 15 min: with Ca2+-free Tyrode and thereafter f or 30 min of reperfusion with normal Tyrode. The 'high energy phosphate com pound' levels were monitored by P-31-NMR, creatine kinase (CK) release was measured in the perfusate. Ca-45 influx was estimated in the papillary musc le. We observed that in the rat heart: (a) high energy phosphate levels dec lined 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. Tn the hamster heart, there was preservation of high energ y phosphates, CK release was prevented completely and no rise in Ca-45 infl ux was observed upon Ca2+ reperfusion. These results suggest that the hamst er heart has a remarkable capacity for Ca2+ homeostasis which protects the heart from Ca2+ overload. (C) 2000 Academic Press.