Preedy V R, Richardson P J
Rayne Institute, Department of Clinical Biochemistry, London.
Herz. 1996 Aug;21(4):241-7.
In this review we survey the features of alcohol-induced lesions in the heart, in both the clinical and laboratory-animal setting. The data indicates a diverse range of lesions that contribute to the genesis of the entity alcoholic cardiomyopathy (also referred to as alcoholic heart muscle disease). Biopsies of affected patients reveal lesions similar to dilated cardiomyopathy though quantitative morphometry can distinguish between the two disorders. Biochemical analysis reveals an increase in the activities of some enzymes, though the pathogenetic nature of these alterations are unknown, but may well be adaptive. The induction of ischaemia in acute ethanol exposure may contribute to the heart muscle damage, though long term experimental studies indicate that heat shock proteins are reduced, making the heart more vulnerable to cardiac dysfunction. Changes in the rate of protein turnover induced by alcohol appear to be a central feature in animal studies and it is very likely that similar changes occur in man.
在本综述中,我们调查了临床和实验动物环境下酒精性心脏病变的特征。数据表明存在多种病变,这些病变导致了酒精性心肌病(也称为酒精性心肌疾病)这一实体的发生。受影响患者的活检显示出与扩张型心肌病相似的病变,尽管定量形态学可以区分这两种疾病。生化分析显示某些酶的活性增加,尽管这些改变的致病性质尚不清楚,但很可能是适应性的。急性乙醇暴露诱导的缺血可能导致心肌损伤,尽管长期实验研究表明热休克蛋白减少,使心脏更容易发生心脏功能障碍。酒精引起的蛋白质周转速率变化似乎是动物研究的一个核心特征,而且人类很可能也会发生类似的变化。