再灌注损伤心肌线粒体钙代谢与呼吸功能关系的研究

Mitochondrial calcium metabolism and respiratory function in reperfused myocardium

观察离体缺氧-再灌注兔心肌线粒体钙含量、钙摄取率和不同底物的呼吸耗氧量的变化。结果表明:缺氧组心肌线粒体钙含量轻度增加(3.37±0.25nmol/mg pr,P<0.05),钙摄取率无显著变化,以琥珀酸为底物的呼吸耗氧量代偿性增高(226.0±28.7natoms/min/mg Pr,P<0.05),以谷氨酸加苹果酸为底物时变化不显著;再灌注组心肌线粒体钙含量显著增高(6.10±1.12nmol/mgt pr,P<0.01);钙摄取率和以谷氨酸加苹果酸为底物的呼吸耗氧量显著降低(P<0.01),且与线粒体钙含量呈显著负相关(r=-0.73,P<0.001),提示线粒体钙超载在再灌注损伤线粒体功能损害中起重要作用。

Mitochondrial calcium content, calcium uptake and oxygen consumption during respiration supported by different substrates were studied on isolated rabbit hypoxic reperfused hearts. The results demonstrated that in hypoxia group, mitochondrial calcium content slightly increased (3.37±0.25nmol/mgMtPr, P<0.05) without significant change in calcium uptake. The oxygen consumption increased (226.0±28.7natoms/min/mgMt Pr, P<0.05) compensatively during succinate supported respiration while no significant change during glutamate-malate Supported respiration. In reperfusion group, mitochondrial calcium content significantly increased (6.10±1.12nmol/mgMt Pr, P<0.01) with significent decreases in calcium uptake and respiratory oxygen consumption of Glut-Mal Supp group (P<0.01). The decrease rates were highly negatively correlated with mitochondrial calcium content (r=-0.73, P<0.001), suggesting the important effect of mitochondrial calcium overload in mitochondrial dysfunction during myocardial reperfusion injury.