败血症大鼠肝、肾、心、肺线粒体功能的变化

Changes of mitochondria functions of liver, kidney, heart, and lung of rats during sepsis

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。

Sepsis model was established by cecum ligation and puncture (CLP) inrats according to Wichterman's method and mitochondria functions of liver, kidney,heart, and lung were observed during early and late stage of sepsis. Respiratory controlrate (RCR) of mitochondria in liver, kidney, and heart were decreased (P<0.001, P<0.05, P<0.01, respectively, vs control value) 12h after CLP. RCR of mitochondria inlung was decreased (P<0.001) and P/O ratio of mitochondria was lowed significantly(P<0.001) 16h after CLP, when compared with control value. At 20h after CLP, RCRand P/O ratio of mitochondria in all the above mentioned organs were decreased evenmore (P<0.001, vs control value). These results suggested that there might be extensiveand severe injury in the vital organ mitochondria during CLP sepsis. Damage of the vitalorgan mitochondria might be the first stage of mutiple organ failure in sepsis which wasrelated to direct actions of bacteria and/or endotoxin.