Nuzhnyi V P, Ugriumov A I, Beliaeva N Y, Zabirova I G, Abdrashitov A K, Paukov V S, Uspenskii A E
Laboratory of Toxicology, All-Union Narcological Research Centre, Moscow, USSR.
Cor Vasa. 1989;31(5):402-10.
Using histochemical methods, light and electron microscopy, authors examined rat heart 2-6 hours, 1, 3, and 7 days after discontinuation of forced intoxication with alcohol. At the same time, they assessed the contractile function and creatine phosphokinase (CPK) activity in the isolated perfused heart, and the development of animal destruction. Ethanol withdrawal was followed by escalation of vascular disorders in the heart, dystrophic changes in the subcellular structures, considerable polymorphism in enzyme distribution and activity, and formation of foci containing disintegrating myocytes with contractures. The contractile function was impaired and CPK release increased in the isolated heart. The changes were most marked 3 days after ethanol discontinuation to disappear after 7 days. Two to seven days after ethanol cessation, 13.1% of rats perished. Cardiac injury due to alcohol withdrawal syndrome may be one of the factors leading to the development of alcohol cardiomyopathy and a cause of sudden death in patients with documented alcohol abuse.
作者运用组织化学方法、光镜和电镜技术,在大鼠被迫停止酒精中毒后2至6小时、1天、3天和7天对其心脏进行了检查。与此同时,他们评估了离体灌注心脏的收缩功能和肌酸磷酸激酶(CPK)活性,以及动物的病变发展情况。停止摄入乙醇后,心脏血管紊乱加剧,亚细胞结构出现营养不良性变化,酶的分布和活性存在显著多态性,并且形成了含有挛缩性崩解心肌细胞的病灶。离体心脏的收缩功能受损,CPK释放增加。这些变化在停止摄入乙醇后3天最为明显,7天后消失。停止摄入乙醇后2至7天,13.1%的大鼠死亡。酒精戒断综合征导致的心脏损伤可能是酒精性心肌病发展的因素之一,也是有酗酒记录患者猝死的一个原因。