尿毒症大鼠心肌超微结构和细胞内钙离子代谢的变化

为研究实验性尿毒症大鼠心肌超微结构，以及心肌细胞琥珀酸脱氢酶（SDH）和细胞内游离Ca^2 变化对膜通道的影响，通过制作尿毒症大鼠模型，采用定量细胞酶活性的化学方法观察了SDH活性变化，用共聚焦激光扫描显微镜观察细胞膜Ca^2 通道。结果显示，随着尿毒症病情进展，心肌细胞膜卷曲，破裂，肌原纤维肿胀，裂解，有SDH反应产物的线粒体数量明显减少，细胞膜Ca^2 通道活性明显增加，胞浆内钙离子蓄积。提示尿毒症时心肌细胞膜扣伤，线粒体功能酶含量降低，细胞内钙超载是导致心功能异常的病理生理基础。

THE CHANGES OF MYOCARDIAL ULTRASTRUCTURE AND CELL MEMBRANE CHANNEL IN UREMIC RATS

The aim of this study was to explore the myocardial ultrastructure of experimental uremic rats and the effect of myocardiocyte succinate dehydrogenase(SDH) and free cytosolic calcium changes on membrane channel. By making a uremia model in rats, changes of SDH activation was observed by quantitative enzyme cytochemistry methods and membrane calcium channel was checked by laser scanning confocal microscopy. The results showed that with the uremia becoming heavier, myocardiocyte membrane was rolled and broken, myofibrils were swollen and broken. The quantity of mitochondria with SDH products significantly decreased, while activation of cell membrane calcium channel markedly increased and cytosolic calcium piled up. It is suggested that impaired myocardial membrane, decreased contents of mitochondrial function enzyme and cytosolic calcium overload are the pathophisiological basis leading to cardiac dysfunction in uremia.