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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。
In this paper, the changes of electron transport activity and cytochrome content in the respiratory chain of rat liver mitochondria during hemorrhagic shock were studied. The results showed that hemorrhagic shock caused by mitochondrial electron transport activity decreased: shock 2hNADH cytochrome c reductase was significantly lower than the sham group; shock 3hNADH-Co. Q reductase, succinate-Co. Q reductase, succinate - cytochrome c reductase and cytochrome oxidase were significantly lower than the sham group, and with the shock process decreased. In addition, the mitochondrial cytochrome c content in liver was significantly decreased 2 h after shock, while the cytochromes a, b and c1 also significantly decreased at 4 h after shock. These results suggest that, in addition to low-flow hypoxia, hemorrhagic shock-induced mitochondrial respiratory dysfunction is associated with the decreased ability of mitochondria to utilize oxygen; and the decreased electron transport activity of the respiratory chain of mitochondrial inner membrane may have a structural change with the mitochondrial inner membrane And cytochrome lost.