Kaminishi K, Yanagishita T, Kako K J
Department of Physiology, University of Ottawa, School of Medicine, Ontario.
Can J Cardiol. 1989 Apr;5(3):168-74.
Recent evidence suggests that free radicals are generated in the heart during the reperfusion which follows ischemia. Intracellular accumulation of calcium has been postulated to be an important pathogenic factor in a number of disease states, including reperfusion injury. Therefore, in this study, the effects of various oxidants on calcium uptake by isolated rat heart cells were investigated. Ammonium persulphate, t-butyl hydroperoxide and phenazine methosulphate increased the number of cells in contracture in both a concentration dependent and time dependent manner, while 45Ca content of cardiomyocytes was decreased by oxidant in proportion to its concentration. Carbonyl cyanide m-chlorophenyl-hydrazone (CCCP) dependent (mitochondrial) and CCCP independent (sarcoplasmic reticulum) 45Ca contents in chemically skinned myocytes were reduced by the oxidants. By contrast, hydrogen peroxide raised 45Ca content of cardiomyocytes and did not reduce sarcoplasmic reticulum 45Ca content, although mitochondrial 45Ca content was decreased. Release of 45Ca from mitochondria and sarcoplasmic reticulum in saponin treated myocytes was accelerated by hypochlorous acid and hydrogen peroxide. The authors conclude that oxidants other than hydrogen peroxide inhibited intracellular uptake of calcium and accelerated calcium release, thus raising the cytosolic calcium concentration and causing cell contracture. The net influx of calcium across sarcolemmal membrane was decreased by these oxidants.
最近有证据表明，在缺血后的再灌注过程中，心脏会产生自由基。细胞内钙的积累被认为是包括再灌注损伤在内的多种疾病状态中的一个重要致病因素。因此，在本研究中，研究了各种氧化剂对分离的大鼠心脏细胞钙摄取的影响。过硫酸铵、叔丁基过氧化氢和吩嗪硫酸甲酯以浓度和时间依赖性方式增加挛缩细胞的数量，而氧化剂使心肌细胞的45Ca含量与其浓度成比例下降。氧化剂降低了化学去表皮心肌细胞中依赖羰基氰化物间氯苯腙（CCCP）的（线粒体）和不依赖CCCP的（肌浆网）45Ca含量。相比之下，过氧化氢增加了心肌细胞的45Ca含量，并且没有降低肌浆网的45Ca含量，尽管线粒体的45Ca含量有所下降。次氯酸和过氧化氢加速了皂素处理的心肌细胞中线粒体和肌浆网的45Ca释放。作者得出结论，除过氧化氢外的氧化剂抑制细胞内钙摄取并加速钙释放，从而提高细胞质钙浓度并导致细胞挛缩。这些氧化剂减少了钙跨肌膜的净内流。
