热应激心肌细胞损伤的线粒体机制探讨

目的：观察热应激对大鼠凡肌细胞线粒体氧化磷酸化和钙代谢功能的影响、研究线粒体膜渗透性转移（ＰＴ）的变化及其病理学意义、探索热应激心肌细胞损伤发生机制。方法：用Ｋｌａｒｋ氧电极极谱法测定线粒体呼吸功能，用生物发光法主肌ＡＴＰ含量及线粒体Ｃａ＾２＋。ＡＴＰ酶活性；用电感耦合等离子－原子发射光谱仪测定线粒体内Ｃａ＾２＋含量，用分光光度法测定线粒体膜ＰＴ。结果：热应激大鼠心肌细胞线粒体的呼吸控制率（ＲＣＰ

MITOCHONDRIAL MECHANISM OF HEAT STRESS-INDUCED INJURY IN RAT CARDIOMYOCYTE

Aim: In order to elucidate the mechanism of cardiomyocyte injury in heat stress, the changes of oxidative phosphorylation and calcium metalolism in cardiac mitochondria of heatexposed Wistar rats were observed. The changes of mitochondrial permeability transition and its pathological significance were studied as well. Methods: The respiratory function of mitochondria was measured by Klark oxgenelectrode polarography; Myocardial ATP content and activity of Ca 2 ATPase in mitochondria were analyzed with bioluminescent method; Mitochondrial Ca 2 content was assayed by ICP; PT was measured using spectrophotometer. Results: The respiratory control rate (RCR) and oxidative phosphorylation efficiency (P/O) were decreased gradually as rectal temperature (Tr) increased. The activity of Ca 2 ATPase and Ca 2 content were also reduced. Exposing to the Ca 2 overload and oxidative stress, mitochondrial PT altered markedly. Ruthenium red and SOD could prevent the changes of mitochondrial PT. Conclusion: Destruction of mitochondrial structure and function may be of great significance in the development of impaired cardiac function in the heat stress.