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[完全缺血和3',5'-环磷酸腺苷对大鼠心脏线粒体中Ca2+离子转运热稳定细胞质抑制剂活性的影响]

[Effect of total ischemia and 3',5'-cAMP on the activity of the thermostable cytoplasmic inhibitor of Ca2+ ion transport in rat heart mitochondria].

作者信息

Turakulov Ia Kh, Luchenko M B, Gaĭnutdinov M Kh, Abidov A A

出版信息

Vopr Med Khim. 1985 Jan-Feb;31(1):85-9.

PMID:2984845
Abstract

Activity of cytoplasmic inhibitor of Ca2+ transport in rat heart mitochondria was studied after total ischemia and incubation of heart homogenates with cAMP. Distinct inactivation of the inhibitor occurred under these conditions. The decrease of the inhibitor activity in ischemic myocardium appears to serve as a compensatory mechanism: 1. pyruvate dehydrogenase and the enzymes of tricarboxylic acid cycle were activated due to increase in Ca2+ concentration in mitochondria, 2. as a result of Ca2+ accumulation in mitochondria the elevated concentration of Ca2+ was decreased in myoplasm, which developed after impairment of plasmatic membranes and of sarcoplasmic reticulum membranes.

摘要

在大鼠心脏线粒体中，研究了总缺血以及心脏匀浆与环磷酸腺苷（cAMP）孵育后钙离子转运胞质抑制剂的活性。在这些条件下，抑制剂发生了明显的失活。缺血心肌中抑制剂活性的降低似乎是一种代偿机制：1. 由于线粒体中钙离子浓度增加，丙酮酸脱氢酶和三羧酸循环的酶被激活；2. 由于线粒体中钙离子的积累，肌浆中升高的钙离子浓度降低，这是在质膜和肌浆网膜受损后出现的。

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