失血性休克时大鼠肝线粒体内膜的损伤  

Hemorrhagic shock-induced damages in the inner membrane of rat liver mitochondria

作　　者：缪明永[1] 朱善宏[1,2] 石汉平[1,3] 陈克明[1] 

机构地区：[1]上海第二军医大学生物化学教研室 [2]南京军区福州医学高等专科学校生物化学教研室 [3]广州南方医院普外科

出　　处：《中国病理生理杂志》1995年第1期86-89,共4页Chinese Journal of Pathophysiology

摘　　要：本文研究失血性休克时鼠肝线粒体内膜呼吸链电子传递活性和细胞色素含量的改变。结果表明失血性休克引起线粒体电子传递活性不断下降：休克２ｈＮＡＤＨ－细胞色素ｃ还原酶显著低于假处理组；休克了３ｈＮＡＤＨ－Ｃｏ．Ｑ还原酶，琥珀酸－Ｃｏ．Ｑ还原酶，琥珀酸－细胞色素ｃ还原酶以及细胞色素氧化酶均明显低于假处理组，并随休克进程不断降低。另外，休克２ｈ肝线粒体细胞色素ｃ含量明显减少，而细胞色素ａ、ｂ，ｃ１在休克４ｈ也明显减少。上述结果提示失血性休克引起线粒体呼吸功能障碍除了与低流性缺氧有关外，还与线粒体利用氧的能力下降有关；而线粒体内膜呼吸链电子传递活性下降可能与线粒体内膜发生了结构改变和细胞色素丢失有关。The electron transport chain alterations and cytochromes content in livermitochondria of rat with hemorrhagic shock were studied.The results showed thathemorrhagic shock let to progressive decrease of the activities of two respiratory chains.At 2h after shock,NADH-cytochrome c reductase declined significantly as comparedwith that of the sham-operated,and at 3h following shock,succinate-Co.Q reductase,succinate-cytochrome c reductase,NADH-Co.Q reductase and cytochrome oxidase weremuch lower than those of the sham-operated.These results suggested that the utilizationof oxygen decrease in liver mitochondria of rat following hemorrhagic shock.In addi-tion, cytochrome c content of liver mitochondria dropped significantly at 2h after shockand cytochrome a,b,c-1 contents also dropped at 4h following shock.These results in-dicated that the impairment took place in liver mitochondria inner membrane. It wassuggested that mitochondria dysfunction is related to two events: low-flow hypoxiaand inability to utilize oxygen, and that declining activities of electron transport mightbe due to impairment of mitochondria inner membrane and lost of cytochromes.

关 键 词：休克 失血性 线粒体 肝 氧化磷酸化 大鼠 损伤 

分 类 号：R541.640.2[医药卫生—心血管疾病]