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本实验根据Wichterman等人方法建立盲肠结扎穿孔(CLP)败血症大鼠模型,观察了CLP败血症早、晚期心、肺、肝和肾线粒体功能的变化。CLP12h,肝、肾和心线粒体呼吸控制率(RCR)较对照组明显降低(分别为P<0.001,P<0.05,P<0.01)。CLP16h,肺线粒体RCR亦有明显降低(P<0.001)。各生命脏器线粒体P/O值也都较对照组显著下降(P<0.001)。CLP20h,RCR和P/O都下降更甚。结果提示CLP败血症过程中,生命脏器线粒体损伤的广泛性和严重性,生命脏器线粒体损伤可能是败血症过程中多种器官功能衰竭的始动环节,线粒体的损伤可能与细菌和/或内毒素的直接作用有关。
In this study, we established a rat model of cecal ligation and puncture (CLP) sepsis according to the method of Wichterman et al. We observed the changes of mitochondrial function in heart, lung, liver and kidney in early and late sepsis. CLP12h, liver, kidney and mitochondrial respiratory control rate (RCR) was significantly lower than the control group (P <0.001, P <0.05, P <0.01). CLP16h, lung mitochondrial RCR also significantly reduced (P <0.001). The mitochondrial P / O values of all living organs were also significantly lower than those of the control group (P <0.001). CLP20h, RCR and P / O are even worse. The results suggest that the severity and severity of mitochondrial damage in vital organs during CLP sepsis and the mitochondrial damage of vital organs may be the initiators of various organ failure during sepsis. Mitochondrial damage may be related to bacterial and / or endotoxin The direct effect of.