Halothane Protects the Isolated Rat Myocardium Against Excessive Total Intracellular Calcium and Structural Damage During Ischemia and Reperfusion

Abstract
Present study was to evaluate the effect of halothane on the total intracellular calcium (Ca2+) content and on myocardial structure both at the end of normothermic cardioplegic arrest and at the end of reperfusion. Isolated perfused rat hearts were perfused for a control period of 30 min, followed by 40 min of normothermic cardioplegic 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 evaluated by electron microscopy. Grading of ischemic damage showed that exposure to normothermic cardioplegia resulted in marked ischemic injury, regardless of whether the hearts were treated with halothane. Reperfusion in the presence of halothane caused a significant reversal of ischemic damage and almost complete ultrastructural repair, whereas untreated hearts still exhibited severe edema, contracture, and contracture bands. 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 this protective action is under investigation. Address correspondence to Amanda Lochner, PhD, DSc, MRC Programme for Experimental Biology, P.O. Box 19063, Tygerberg 7505, Republic of South Africa. This work was supported by the South African Medical Research Council and the Harry Crossley Foundation. Accepted for publication March 29, 1994. © 1994 International Anesthesia Research Society...

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