Schreiber S S, Oratz M, Rothschild M A
Recent Adv Stud Cardiac Struct Metab. 1975;7:431-42.
The occurrence of cardiomy opathy in chronic alcoholics is well known, but the causes are as yet unclear (Mitchell and Cohen, 1970). Metabolic effects of ethanol, such as accumulation of triglycerides despite a decrease in fatty acid extraction (Regan et al., 1966; 1969), have been suggested as a cause of ultimate impairment of myofibrillar function. The suggestion has also been made that the detrimental effects of ethanol may actually be an acetaldehyde effect, mediated through the release of norepinephrine causing chronic chronotropic and inotropic effects which may often play a role in the development of the myopathy (James and Bear, 1967). It has been reported that acute exposure to alcohol decreases to one-third that of the control the capacity of the liver to synthesize albumin (Rothschild et al., 1971). In view of the rapid inhibitory effect, it was felt to be of interest to study the effect of alcohol in the perfused heart to see whether myocardial protein synthesis was similarly inhibited. In addition, since alcohol is apparently not metabolized by the heart (Gailis and Verdy, 1971; Lochner, Cowley, and Brink, 1969). The effect of a primary metabolite, acetaldehyde (James and Bear, 1967), synthesized in liver was also studied. The results indicated that acute exposure to levels of alcohol which decreased albumin synthesis in the perfused liver had no effect on protein synthesis in the perfused heart. However, acetaldehyde, at levels that produce a marked chronotropic and inotropic effect, markedly inhibited protein synthesis of total cardiac protein. To further define the inhibition of protein synthesis by acetaldehyde, the effects of ethanol and acetaldehyde on cardiac micorsomes were also studied in cell-free systems. Some of these data were reported previously (Schreiber et al., 1972; 1974).
慢性酒精中毒患者中发生心肌病是众所周知的，但病因尚不清楚（米切尔和科恩，1970年）。乙醇的代谢作用，如尽管脂肪酸摄取减少但甘油三酯仍会积累（里根等人，1966年；1969年），已被认为是肌原纤维功能最终受损的原因。也有人提出，乙醇的有害作用实际上可能是乙醛的作用，通过去甲肾上腺素的释放介导，引起慢性变时性和变力性作用，这可能在肌病的发展中经常起作用（詹姆斯和贝尔，1967年）。据报道，急性接触酒精会使肝脏合成白蛋白的能力降至对照组的三分之一（罗斯柴尔德等人，1971年）。鉴于这种快速的抑制作用，研究酒精对灌注心脏的影响，以观察心肌蛋白合成是否同样受到抑制，被认为是有意义的。此外，由于心脏显然不代谢酒精（盖利斯和韦迪，1971年；洛赫纳、考利和布林克，1969年）。还研究了在肝脏中合成的主要代谢产物乙醛（詹姆斯和贝尔，1967年）的作用。结果表明，急性接触降低灌注肝脏中白蛋白合成水平的酒精对灌注心脏中的蛋白合成没有影响。然而，产生明显变时性和变力性作用水平的乙醛显著抑制了总心脏蛋白的合成。为了进一步确定乙醛对蛋白合成的抑制作用，还在无细胞系统中研究了乙醇和乙醛对心脏微粒体的影响。其中一些数据先前已有报道（施赖伯等人，1972年；1974年）。
