Bing R J
Circulation. 1978 Dec;58(6):965-70. doi: 10.1161/01.cir.58.6.965.
Changes in cardiac metabolism in myocardial failure and after alcohol ingestion are discussed. The main effect of alcohol ingestion is loss of cardiac contractility. Since heart muscle does not contain alcohol dehydrogenase, its toxicity is probably the result of a direct toxic effect of ethanol and acetaldehyde on the myocardial cell, possibly involving various membrane systems. Alcohol inhibits mitochondrial respiration and the activity of enzymes in the tricarboxylic acid cycle, and its interferes with both mitochondrial calcium uptake and binding. Ethanol profoundly affects myocardial lipid metabolism. Acetaldehyde diminishes myocardial protein synthesis and inhibits Ca++-activated myofibrillar ATPase. In myocardial failure, a series of possibilities may be responsible for the loss of contractility. Excitation-contraction coupling could be disturbed at the level of the sarcolemma, at the sarcoplasmic reticulum, at the mitochondria, and between calcium and the regulatory proteins. Deficiencies in Ca++ delivery systems of excitation-contraction coupling on the myosin ATPase activity could be responsible for the dimunition in cardiac contractility. Mitochondrial function may also be involved, since mitochondria from failing human hearts are defective with respect to respiratory control and calcium accumulation. Under certain conditions, the relationship of mitochondria to calcium sequestration is very important in influencing contractility. The involvement of contractile and regulatory proteins in myocardial failure cannot be excluded.
本文讨论了心肌衰竭及酒精摄入后心脏代谢的变化。酒精摄入的主要影响是心脏收缩力丧失。由于心肌中不含乙醇脱氢酶，其毒性可能是乙醇和乙醛对心肌细胞直接毒性作用的结果，可能涉及各种膜系统。酒精抑制线粒体呼吸和三羧酸循环中酶的活性，并干扰线粒体对钙的摄取和结合。乙醇对心肌脂质代谢有深远影响。乙醛减少心肌蛋白质合成并抑制钙激活的肌原纤维ATP酶。在心肌衰竭中，一系列因素可能导致收缩力丧失。兴奋 - 收缩偶联可能在肌膜、肌浆网、线粒体以及钙与调节蛋白之间受到干扰。兴奋 - 收缩偶联的钙传递系统缺陷以及肌球蛋白ATP酶活性降低可能导致心脏收缩力减弱。线粒体功能也可能参与其中，因为衰竭人类心脏的线粒体在呼吸控制和钙积累方面存在缺陷。在某些情况下，线粒体与钙螯合的关系对影响收缩力非常重要。不能排除收缩蛋白和调节蛋白参与心肌衰竭的可能性。
