부산대학교 도서관

Endothelin(ET), is the most potent endogenous vasoconstrictor. Myocardial ischemia and chemical stimuli including calcium ionophores are known to release ET-1. Recently, halothane has been shown to block calcium channel. Thus, halothane might attenuate coronary endothelial ET-1 production during myocardial ischemia-reperfusion. To test this hypothesis, we measured plasma ET-1 level continuously in open chest dogs subjected to 15 min of left anterior coronary arterial occlusion and 1 hour of reperfusion during fentanly(n=8) or halothane(n=7) anesthesia. The results were as follows. I) Baseline ET-1 levels of both femoral artery and great cardiac vein in the halothane group were lower than in the fentanly group(NS). 2) ET-1 level of femoral artery and great coronary vein in both halothane and fentanyl group remained unchanged 10 min into ischemia. 3) Coronary blood flow increased by 325, 250% in the halothane group and by 315, 258% in the fentanly group 2, 5 min into reperfusion, respectively. 4) ET-1 production increased from baseline of -2.9±1.7 pg/min to 66.0±21.5(p<0.05), 20.8±5.1 (p<0.01), 13.2±6.2(p<0.05) pg/min 5, 15, 30 min into reperfusion, respectively in the fentanyl group, but it remained unchanged from baseline of 0.8±3.1 pg/min in the halothane group. These findings suggest that ET-1 production or release is diminished by halothane during myocardial ischemia-reperfusion. Thus, halothane provides an advantage over fentanyl in patients with myocarial ischemic episodes