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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。
To investigate the role of myocardial mitochondrial calcium regulation in cardiomyocyte calcium overload in shock rats. In the present study, we observed that the mitochondrial calcium content increased by 180% and 330% in the early and late stage of shock, and the mitochondrial calcium transport capacity in shock decreased significantly (the amount of calcium decreased by 34.6% and the rate of calcium intake Decreased by 33%, P <0.01). The results suggest that the reduction of myocardial mitochondrial calcium transport may be one of the important causes of cardiac calcium overload in shock animals, which in turn leads to cardiac dysfunction.