Sevoflurane and isoflurane do not enhance the pre- and postischemic eicosanoid production in guinea pig hearts

Eicosanoids and volatile anesthetics can influence cardiac reperfusion inju ry. Accordingly, we analyzed the effects of sevoflurane and isoflurane appl ied in clinically relevant concentrations on the myocardial production of p rostacyclin and thromboxane A(2) (TxA(2)) and on heart function. Isolated g uinea pig hearts, perfused with crystalloid buffer, performed pressure-volu me work. Between two working phases, hearts were subjected to 15 min of glo bal ischemia followed by reperfusion. The hearts received no anesthetic, 1 minimum alveolar anesthetic concentration (MAC) isoflurane (1.2 vol%), or 0 .5 and 1 MAC sevoflurane (1 vol% and 2 vol%), either only preischemically o r pre- and postischemically. In additional groups, cyclooxygenase function was examined by an infusion of 1 mu M arachidonic acid (AA) in the absence and presence of sevoflurane. The variables measured included the myocardial production of prostacyclin, TxA(2) and lactate, consumption of pyruvate, c oronary perfusion pressure, and the tissue level of isoprostane 8-iso-PGF(2 alpha). External heart work, determined pre- and postischemically, served to assess recovery of heart function. Volatile anesthetics had no impact on postischemic recovery of myocardial function (50%-60% recovery), perfusion pressure, lactate production, or isoprostane content. Release of prostacyc lin and TxA(2) was increased in the early reperfusion phase 5-8- and 2-4-fo ld, respectively, indicating enhanced AA liberation. Isoflurane and sevoflu rane did not augment the eicosanoid release. Only 2 vol% sevoflurane applie d during reperfusion prevented the increased eicosanoid formation in this p hase. Infusion of AA increased prostacyclin production approximately 200-fo ld under all conditions, decreased pyruvate consumption irreversibly, and m arkedly attenuated postischemic heart work (25% recovery). None of these ef fects were mitigated by 2 vol% sevoflurane. In conclusion, only sevoflurane at 2 vol% attenuated the increased liberation of AA during reperfusion. De creased eicosanoid formation had no effect on myocardial recovery in our ex perimental setting while excess AA was deleterious. Because eicosanoids inf luence intravascular platelet and leukocyte adhesion and activation, sevofl urane may have effects in reperfused tissues beyond those of isoflurane. Im plications: In an isolated guinea pig heart model, myocardial eicosanoid re lease was not increased by isoflurane or sevoflurane, either before or afte r ischemia. Sevoflurane (2 vol%) but not isoflurane attenuated the increase d release of eicosanoids during reperfusion.