缺血再灌注损伤对兔心肌线粒体钙稳态的影响

目的:观察心肌在高钾停搏液保护下经历缺血再灌注损伤时,其线粒体钙稳态的变化.方法:采用改良Langendorff离体灌注兔心脏模型,用高钾停搏液停跳停止灌注1 h后再灌注30 min.电镜观察线粒体的变化,分离心肌线粒体并负载钙离子敏感荧光试剂Fura 2-AM,测定线粒体基质游离钙浓度以及线粒体在高钙环境中摄钙能力和加入钠离子后的释钙能力.结果:心肌线粒体基质钙离子浓度明显升高,但摄钙和释钙能力基本已恢复正常.电镜下大量线粒体中可见高密度的钙盐沉积,少量线粒体肿胀、嵴消失.结论:在再灌注初期线粒体钙超载一方面是由于生理性的摄钙过程启动,但也有病理性的摄钙过程参与,30 min以后已没有病理性摄钙过程参与,摄钙释钙能力基本正常.具体的病理生理机制仍有待进一步的研究.

Effect of reperfusion injury on rabbit heart mitochondrial calcium homeostas is

Objective:To study heart mitochondrial calcium homeostasis during ischemia- reperfusion under the protection of cardioplegic solution.Methods:Isolated perfused rabbits hearts were subjected to global ischem ia in the presence of cold cardioplegic solution for an hour and reperfused for half an hour.Electron m icroscope was used to observe the change of mitochondrial structure.Heart m itochondria was isolated and Fura2 - AM was used as the indicator of matrix concentration of calcium(Ca2 + ]m) to m easureCa2 + ]m,the intake and outtake ability of the calcium when m itochondria was at high calcium concentration liquid or high natrium concentration liquid.Results:Ca2 + ]m increased significantly but mitochondria was still able to uptake calcium and release calcium of m atrix.There was some electron- dense deposit in mitochondria and the injury of mitochondria could be seen by electron microscope.Conclusion:The reason for mitochondria calcium overload at the beginning of reperfusion include physiological and pathological calcium uptake,which ends after30 min reperfusion under the protection of cardioplegic solution.