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在心肌低氧及复氧过程中所出现的线粒体大量钙聚积的现象近年来一直为人们所关注,但是其产生的机制及其与线粒体损伤的关系却一直不很清楚。本文实验表明在经过40分钟无氧孵育后,离体心肌线粒体表现出:1.在常氧时,心肌线粒体内钙含量随介质中自由钙浓度的升高而显著增加,同时,也伴随着线粒体呼吸功能的损伤。二者呈正相关。2.在无氧时,心肌线粒体可抑制其钙含量随孵育介质中自由钙浓度的升高而增加。即使在很高外钙浓度(10~(-4)M)时仍是如此.与此相应,线粒体呼吸功能损伤的程度随介质中钙浓度的升高也无显著升高。
In recent years, the phenomenon of massive accumulation of calcium in mitochondria, which occurs during myocardial hypoxia and reoxygenation, has been attracting attention for a long time. However, its mechanism and its relationship with mitochondrial damage have not been clearly understood. Our experiments show that after 40 minutes of anaerobic incubation, mitochondria in vitro showed: 1. In normoxia, myocardial mitochondrial calcium content with the free calcium concentration in the media and significantly increased, but also accompanied by mitochondria Respiratory damage. The two are positively correlated. 2. In the absence of oxygen, myocardial mitochondria can inhibit the calcium content with increasing free Ca concentration in the incubation medium and increased. Even at very high calcium concentrations (10 -4 M), the degree of mitochondrial respiratory impairment did not increase significantly with increasing calcium concentration in the medium.