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目的 :观察热应激对大鼠心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换 (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 ,用生物发光法测定心肌ATP含量及线粒体Ca2 +。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Ca2 +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 (RCR)及氧化磷酸化效率 (P/O)均随热应激强度的增强呈显著逐步降低趋势 ;心肌线粒体Ca2 + ATP酶活性和Ca2 +含量亦明显下降 ;暴露于Ca2 +超载和氧化应激状态的线粒体 ,膜PT发生明显变化 ,钌红、抗氧化剂及反应体系酸化状态的纠正能够有效阻抑PT变化。结论 :线粒体结构与功能的破坏在热应激机体心功能损伤的发生中有着极其重要的意义。
OBJECTIVE: To observe the effects of heat stress on mitochondrial phosphorylation and calcium metabolism in rat cardiac myocytes, investigate the changes of mitochondrial membrane permeability transition (PT) and its pathological significance, and explore the mechanism of heat-induced cardiomyocyte injury. Methods: Mitochondrial respiratory function was measured by Klark oxygen electrode polarography. ATP content and mitochondrial Ca2 + were measured by bioluminescence method. ATPase activity. The content of Ca2 + in mitochondria was determined by inductively coupled plasma atomic emission spectrometry. The mitochondrial membrane PT was determined by spectrophotometry. Results: The mitochondria respiratory control rate (RCR) and oxidative phosphorylation efficiency (P / O) of heat-stressed rat myocardial cells decreased significantly with the increase of heat shock intensity. The activities of mitochondrial Ca2 + -ATPase and Ca2 + + Content also significantly decreased; exposed to Ca2 + overload and oxidative stress mitochondria, PT significant changes in the membrane, ruthenium red, antioxidants and reaction system acidification can effectively suppress PT changes. Conclusion: The destruction of mitochondrial structure and function is extremely important in the occurrence of cardiac dysfunction in heat stress.