Zavitaeva I B, Beliaeva N Iu, Paukov V S
Research Center of Drug Control, Medical Academy, Moscow, Russia.
Arkh Patol. 1995 Nov-Dec;57(6):15-21.
An experimental study of alcoholic heart damage was performed in 150 male rats of series I, II and III with modelled acute alcoholic intoxication, chronic alcoholic intoxication against developing abstinence syndrome, alcoholic abstinence syndrome, respectively. The degree of cardiomyocyte damage is largely determined by structural changes of histohematic barriers in alcoholic intoxication. Primary ethanol damage of the microcirculatory bed, that of perivascular connective tissue and sarcolemma result in a cardiomyocyte mitochondria damage and development of energetic deficiency. Atrophic and sclerotic alterations of the histohematic barrier develop in chronic alcoholic intoxication resulting in profound metabolic changes in the heart muscle and development of alcoholic cardiomyopathy. The damages to the histohematic barrier in abstinence syndrome result in catecholamine penetration into cardiomyocytes and development of focal necrosis in the myocardium.
对第I、II和III组的150只雄性大鼠进行了酒精性心脏损伤的实验研究，分别模拟急性酒精中毒、对抗戒酒综合征发展的慢性酒精中毒、酒精戒断综合征。心肌细胞损伤程度在很大程度上取决于酒精中毒时组织血液屏障的结构变化。微循环床、血管周围结缔组织和肌膜的原发性乙醇损伤导致心肌细胞线粒体损伤和能量缺乏的发展。慢性酒精中毒时组织血液屏障会出现萎缩和硬化改变，导致心肌发生深刻的代谢变化和酒精性心肌病的发展。戒酒综合征时组织血液屏障的损伤导致儿茶酚胺渗入心肌细胞，进而导致心肌局灶性坏死。
