Halothane suppresses the increase in intracellular calcium concentration of isolated rat myocytes during hydrogen peroxide perfusion.

Ischemia-reperfusion injury is probably caused by the generation of oxygen free radicals. The final common pathway to cell injury may be mediated by intracellular calcium overloading induced by oxygen free radicals. Volatile anesthetics have been shown to improve myocardial function following reperfusion. To determine whether or not oxygen radicals are involved in the mechanism by which volatile anesthetics improve myocardial function following reperfusion, we investigated the effects of hydrogen peroxide (H2O2) on the intracellular calcium concentration ([Ca2+]i) in isolated rat ventricular cells. First, the effects of volatile anesthetics, halothane, isoflurane, or sevoflurane, on [Ca2+]i were studied in the absence of H2O2. Next, myocytes were perfused with volatile anesthetics in the presence of H2O2. [Ca2+]i was measured using fura-2, a Ca2+-sensitive fluorescent dye. None of the volatile anesthetics changed [Ca2+]i in the absence of H2O2. In the presence of H2O2, [Ca2+]i gradually increased during H2O2 perfusion. Halothane delayed the onset of the increase in [Ca2+]i induced by H2O2, whereas sevoflurane and isoflurane accelerated the onset. Furthermore, sevoflurane caused more pronounced accumulation of intracellular calcium than did halothane and isoflurane. Therefore, the reduction of excessive intracellular calcium accumulation caused by halothane may have beneficial effects on myocardial function following reperfusion.