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实验性冠状动脉供血不足时心肌肌浆网膜中的肌酸磷酸激酶活性

[Creatine phosphokinase activity in myocardial sarcoplasmic reticulum membranes in experimental coronary insufficiency].

作者信息

Frol'kis R A, Voronkov G S, Dubur G Ia, Tsiomik V A, Gomon I V

出版信息

Biull Eksp Biol Med. 1983 May;95(5):53-5.

PMID:6850090
Abstract

Experiments on rats with acute coronary blood flow restriction (intravenous injection of vasopressin in a dose of 0.5 units/kg) have shown a decrease in the activity of creatine phosphokinase (CPK) and activation of lipid peroxidation in sarcoplasmic reticulum (SPR) membranes. These changes were attended by structural abnormalities in the membrane apparatus of the SPR, primarily on the part of the lipid composition. Pretreatment (1 h before vasopressin) of the animals with the antioxidant AV-156Na averted the development in the SPR membranes of the changes described. This evidences that the rate of peroxide reactions in the myocardium might determine in many respects the metabolic and structural supply of the cell apparatus.

摘要

对大鼠进行急性冠状动脉血流受限实验(静脉注射剂量为0.5单位/千克的加压素),结果显示肌酸磷酸激酶(CPK)活性降低,肌浆网(SPR)膜中的脂质过氧化作用激活。这些变化伴随着SPR膜装置的结构异常,主要体现在脂质组成部分。用抗氧化剂AV - 156Na对动物进行预处理(在注射加压素前1小时)可避免上述SPR膜变化的发生。这证明心肌中过氧化物反应的速率在很多方面可能决定细胞装置的代谢和结构供应。

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