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左心室缺血性挛缩(“石心”)的超微结构

Ultrastructure of ischemic contracture of the left ventricle ("stone heart").

作者信息

Lie J T, Sun S C

出版信息

Mayo Clin Proc. 1976 Dec;51(12):785-93.

PMID:994557
Abstract

Myocardial biopsies from two patients who had developed "stone heart" (myocardial rigor mortis; ischemic contracture of the left ventricle) were studied by electron microscopy. The ultrastructure of tissue in stone heart, though ischemic in nature, differed from that of classic myocardial infarction in some respects. Apart from depletion of glycogen and distension of the sarcoplasmic reticulum and T-tubules, myofibrillar degeneration was much more widespread. Mitochondrial degeneration with active lysosomal autodigestion, disruption of the microcirculation, and lymphedema were prominent changes also observed. In the light of known clinical and experimental observations, our findings suggest that stone heart is an accelerated form of ischemic injury occurring in vulnerable (hypertrophied) hearts and is probably related to ischemia-triggered release of endogenous catecholamines.

摘要

对两名出现“石心”(心肌尸僵;左心室缺血性挛缩)的患者进行了心肌活检,并通过电子显微镜进行研究。石心组织的超微结构虽然本质上是缺血性的,但在某些方面与典型心肌梗死不同。除糖原耗竭、肌浆网和T小管扩张外,肌原纤维变性更为广泛。还观察到线粒体变性伴活跃的溶酶体自噬、微循环破坏和淋巴水肿等突出变化。根据已知的临床和实验观察结果,我们的发现表明,石心是在易损(肥厚)心脏中发生的一种加速形式的缺血性损伤,可能与缺血触发的内源性儿茶酚胺释放有关。

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