HALOTHANE PROTECTS THE ISOLATED RAT MYOCARDIUM AGAINST EXCESSIVE TOTAL INTRACELLULAR CALCIUM AND STRUCTURAL DAMAGE DURING ISCHEMIA AND REPERFUSION

A recent study from our laboratory demonstrated halothane to be a powe rful protectant of the isolated rat heart during reperfusion after nor mothermic cardioplegic arrest. It was speculated that this protective effect might be due to prevention of excessive intracellular calcium. The aim of the present study was to evaluate the effect of halothane o n the total intracellular calcium (Ca2+) content and on myocardial str ucture both at the end of normothermic cardioplegic arrest and at the end of reperfusion. Isolated perfused rat hearts were perfused for a c ontrol period of 30 min, followed by 40 min of normothermic cardiopleg ic arrest with or without reperfusion for 30 min. Halothane (1.5%) was administered continuously before and after arrest. Halothane caused a significant decrease of intracellular Ca2+ at the end of normothermic cardioplegic arrest and after reperfusion. Myocardial morphology was assessed by extensive light microscopy and ultrastructure was evaluate d by electron microscopy. Grading of ischemic damage showed that expos ure to normothermic cardioplegia resulted in marked ischemic injury, r egardless of whether the hearts were treated with halothane. Reperfusi on in the presence of halothane caused a significant reversal of ische mic damage and almost complete ultrastructural repair, whereas untreat ed hearts still exhibited severe edema, contracture, and contracture b ands. Our results indicate that the beneficial effects of halothane on myocardial structural recovery during reperfusion is associated with a reduction in excessive intracellular Ca2+ The exact mechanism of thi s protective action is under investigation.