败血症大鼠心肌线粒体钙转运能力的变化

Changes of calcium transport of rat myocardial mitochondria during septic shock

为探讨心肌线粒体钙调节功能在休克大鼠心肌细胞钙超负荷发生中的作用。本文采用结扎大鼠盲肠加穿孔的腹膜炎败血症休克模型,观察到休克早期、晚期线粒体钙含量分别增加180%、330%,休克晚期线粒体钙转运能力明显降低(摄钙量减少34.6%,摄钙速率降低33%,P<0.01)。结果提示,心肌线粒体钙转运能力的降低可能是休克动物心肌钙超负荷,继而导致心功能障碍的重要原因之一。

In oeder to investigate the pathogenetic role of mitochondria in the patho- genesis of intracellular calcium overload in septic rat. The present study observed the cal- cium content and calcium influx into myocardial mitochondria on the early and late sepsis of rat produced by cecal ligature and puncture. The results showed that mitochondrial calcium contents increased markedly in both early (180%) and late (330%) sepsis. The calcium transport capacity of mitochondria in late sepsis decreased dramatically (uptake decreased 34.6%, uptake velocity lowered 33.3%, p<0.01). These data suggested that the Teduction of calcium transport capacity of myocardial mitochondria was one of the main reasons contributes to intracellular calcium overload of cardiac myocytes and conse- quently caused heart failure in septic rat.