不可逆损伤的成年大鼠离体矩形心脏肌细胞对线粒体酶的保留

Mitochondrial enzyme retention by irreversibly damaged rectangular isolated adult rat heart myocytes.

作者信息

Wenger W C, Murphy M P, Kindig O R, Capen C C, Brierley G P, Altschuld R A

出版信息

Life Sci. 1985 Nov 4;37(18):1697-704. doi: 10.1016/0024-3205(85)90297-8.

Abstract

A one hour hypoxic incubation causes the release of a small but significant amount of cytosolic lactic dehydrogenase from glucose-deprived isolated adult rat heart myocytes. However, enzymes associated with the mitochondria are not liberated, and there is no increase in the number of hypercontracted cells. These observations led Piper et al. (Life Sciences 35, 127-134 [1984]) to conclude that reversibly injured myocytes can release cytosolic proteins. This conclusion was based on the supposition that irreversibly hypoxic injury must cause mitochondrial enzyme efflux and hypercontracture. The present study establishes that this supposition is invalid.

摘要

一小时的缺氧孵育会导致葡萄糖缺乏的成年大鼠离体心肌细胞释放少量但显著量的胞质乳酸脱氢酶。然而，与线粒体相关的酶并未释放，并且过度收缩的细胞数量也没有增加。这些观察结果使派珀等人（《生命科学》35卷，127 - 134页[1984年]）得出结论，可逆性损伤的心肌细胞可以释放胞质蛋白。这一结论基于这样的假设，即不可逆性缺氧损伤必定会导致线粒体酶外流和过度收缩。本研究证实这一假设是无效的。