Zannad F, Senn N, Juillière Y, Royer R J
Pathol Biol (Paris). 1985 Jun;33(6):665-71.
The direct effects of ethanol on cardiac contractility are controversial, probably because of methodological reasons in relation to the choice of appropriate experimental models. We studied the direct effects of 1, 2, 5 and 10 g/l ethanol on myocardial performance and metabolism in the isolated perfused working guinea-pig heart. In the normal heart ethanol induced a dose-dependent, fully reversible depression of cardiac contractility without significant changes of heart rate or cardiac metabolism. In the post-anoxic failing heart this effect was more pronounced. Ethanol had no arrhythmogenic effect even at high concentrations. Finally, it had no measurable effect on anoxic-induced alterations or post-anoxic recovery after a period of 20 minutes of anoxic perfusion. However anoxic-induced lactate production was decreased in hearts pretreated with 10 g/l ethanol. These results demonstrate the direct negative inotropic effect and the lack of chronotropic effect of ethanol. They suggest the lack of effect on excitability. The mechanism of the negative inotropic effect does not seem to be metabolically related since cardiac oxygen consumption and lactate production remained unaltered.
乙醇对心脏收缩性的直接影响存在争议,这可能是由于在选择合适实验模型方面的方法学原因。我们研究了1、2、5和10克/升乙醇对离体灌流的豚鼠工作心脏的心肌性能和代谢的直接影响。在正常心脏中,乙醇可引起剂量依赖性、完全可逆的心脏收缩性抑制,而心率或心脏代谢无明显变化。在缺氧后衰竭心脏中,这种作用更为明显。即使在高浓度下,乙醇也没有致心律失常作用。最后,在20分钟缺氧灌流后,乙醇对缺氧诱导的改变或缺氧后恢复没有可测量的影响。然而,用10克/升乙醇预处理的心脏中,缺氧诱导的乳酸生成减少。这些结果证明了乙醇的直接负性肌力作用和缺乏变时作用。它们提示乙醇对兴奋性没有影响。负性肌力作用的机制似乎与代谢无关,因为心脏耗氧量和乳酸生成保持不变。