Ozaki S, Gotoh Y, Nakaya H, Azuma M, Kanno M
Anesth Analg. 1985 Nov;64(11):1060-4.
Electrophysiologic effects of halothane and enflurane in the presence of a normal pH and during metabolic acidosis were examined in isolated rabbit hearts perfused at a constant rate. During exposure to a normal pH, both halothane and enflurane produced concentration-dependent suppression of sinus node automaticity and atrioventricular conduction. Intraatrial and intraventricular conduction times during constant pacing were slightly but significantly prolonged by these anesthetics at 2 MAC. The magnitudes of these electrophysiologic changes were similar with halothane and enflurane when compared at the same MAC. These electrophysiologic effects became more marked during metabolic acidosis (pH 6.9). These results suggest that enflurane and halothane have direct depressant actions on the cardiac conduction system and that these electrophysiologic effects may be augmented by metabolic acidosis.
在恒速灌注的离体兔心脏中，研究了在正常pH值和代谢性酸中毒情况下氟烷和恩氟烷的电生理效应。在暴露于正常pH值期间，氟烷和恩氟烷均产生浓度依赖性的窦房结自律性抑制和房室传导抑制。在2倍最低肺泡有效浓度（MAC）时，这些麻醉药使恒速起搏期间的心房内和心室内传导时间略有但显著延长。当在相同MAC下比较时，氟烷和恩氟烷引起的这些电生理变化幅度相似。在代谢性酸中毒（pH 6.9）时，这些电生理效应变得更加明显。这些结果表明，恩氟烷和氟烷对心脏传导系统有直接抑制作用，并且这些电生理效应可能会因代谢性酸中毒而增强。
