Reduction of Postischemic Contractile Dysfunction of the Isolated Rat Heart by Sevoflurane: Comparison with Halothane

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Abstract
Our aims were to evaluate the effect of sevoflurane on postcardioplegic functional recovery of the isolated rat heart including the role of the adenosine triphosphate regulated potassium (KATP) channels and to compare the cardioprotective effects of equipotent concentrations of halothane and sevoflurane. Isolated perfused rat hearts were subjected to 45 or 60 min normothermic cardioplegic arrest and 30 min reperfusion. Sevoflurane (0.9% and 1.7%), halothane (0.4% and 0.8%), or sevoflurane (0.9%) plus glibenclamide (10 μM) (a KATP channel blocker) were administered at different time intervals. Measurements of mechanical activity were made before and after arrest. Function during reperfusion after cardioplegic arrest was significantly depressed in both untreated and treated hearts. However, sevoflurane administered both before and after arrest, or before only, significantly improved functional recovery after 45 min of cardioplegia. This protective effect was abolished by simultaneous administration of glibenclamide, suggesting a role of the KATP channel. Sevoflurane was as effective as halothane in improving postcardioplegic functional performance. After 45 min of arrest, hearts exposed to either anesthetic at both concentrations had a significantly higher work performance on discontinuation of their administration than untreated controls. After 60 min of arrest, neither anesthetic elicited protection. In view of the possible significance for volatile anesthetics in cardiac surgery, the effects of sevoflurane and halothane were compared on postcardioplegic recovery of rat hearts. Both anesthetics were equally effective in improving functional recovery after normothermic cardioplegic arrest. Sevoflurane’s beneficial effects were abolished by glibenclamide, suggesting a role for the adenosine triphosphate regulated potassium channel.