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机构地区:[1]第二军医大学训练部生物化学教研室,200433
出 处:《第二军医大学学报》1992年第3期212-215,共4页Academic Journal of Second Military Medical University
基 金:军队"七;五"攻关课题基金 (Ⅰ-01-003)
摘 要:作者研究了失血性休克时鼠心肌线粒体呼吸链的损伤,用改良Wigger法复制失血性休克模型,用差速离心法分离心肌线粒体,用氧电极技术和差光谱法测定琥珀酸呼吸链和NADH呼吸链。结果表明随着休克的进行,二条呼吸链的电子传递活力不断下降。休克3h后,琥珀酸-Co.Q还原酶,琥珀酸-Cyt.C还原酶,NADH-Co.Q还原酶,NADH-Cyt.C还原酶和细胞色素氧化酶等活力显著低于假处理组,表明二条呼吸链有明显损伤。提示休克后期除了有低流性缺氧外,还有氧利用障碍。The alterations in electron transport were studied in the myocardial mitochondria of rats with hemorrhagjc shock. Hemorrhagic shock model was induced by a modified Wigger procedure. Mitochondria were obtained by differential centrifugation. Succinate-, and NADH-respiratory chains were assayed by polarographically and spectrophotometrically in isolated myocardial mitochondria. The results showed that hemorrhagic shock led to progressive decrease in the enzymatic activities of two respiratory chains. The activities of Succinate-Co. Q reductase, Succinate-Cyt. C reductase, NADH-Co. Q reductase, NADH-Cty. C reductase and cytochrome oxidase were remarkably lower in shock 3 h group than those in the shamoperated. This implies that there is not only low-flow hypoxia, but inability to utilizer oxygen in the myocardial mitochondria
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