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[急性和慢性实验性酒精中毒中的心肌]

[Myocardium in acute and chronic experimental alcoholic intoxication].

作者信息

Beliaeva N Iu, Paukov V S, Svistukhin A I, Ugriumov A I, Uspenskiĭ A E

出版信息

Arkh Patol. 1982;44(8):25-32.

PMID:6890796
Abstract

The myocardium of both heart ventricles in acute (AAP) and chronic (CAP) alcoholic poisoning was studied in 90 randombred rats. Functional-morphological changes typical of alcoholic cardiomyodystrophy were shown to develop in the heart in AAP and CAP. In AAP, alcoholic cardiomyodystrophy may lead to acute cardiac insufficiency and in CAP to progressive reduction of the contractile function of the heart and disturbances of conductivity in it. In AAP, however, the leading factor is the disturbance of bioenergetics as a result of toxic effect of ethanol and its metabolites on mitochondrial membranes under conditions of markedly disordered microcirculation. In CAP, along disordered microcirculation. In CAP, along with compensatory-adaptative processes in cardiomyocytes there increase the defects of the contractile apparatus, and diffuse fine-focal cardiosclerosis. This is the result of a long-term effect of ethanol and progressive hypoxia due to the affected vessels and disorders in lipid metabolism. Disorders in the function of sarcoplasmic reticulum may contribute to reduced contractile capacity of the heart.

摘要

在90只杂种大鼠中研究了急性(AAP)和慢性(CAP)酒精中毒时两个心室的心肌情况。结果显示,AAP和CAP时心脏出现了酒精性心肌营养不良典型的功能形态学变化。在AAP中,酒精性心肌营养不良可导致急性心功能不全,而在CAP中则导致心脏收缩功能逐渐降低以及心脏传导障碍。然而,在AAP中,主要因素是在微循环明显紊乱的情况下,乙醇及其代谢产物对线粒体膜的毒性作用导致生物能量学紊乱。在CAP中,除了微循环紊乱外,心肌细胞中的代偿适应过程伴随着收缩装置缺陷的增加以及弥漫性细灶性心肌硬化。这是乙醇长期作用以及由于血管受累和脂质代谢紊乱导致的进行性缺氧的结果。肌浆网功能障碍可能导致心脏收缩能力下降。

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