MECHANISMS OF MYOCARDIAL REPERFUSION INJURY

铁介导的活性氧心肌损伤机制研究进展 代谢物将在培养的心肌细胞中进行研究， 心和完好无损的狗。培养的心肌细胞将暴露在氧气中 代谢产物或活化的中性粒细胞与细胞膜的时间进程 损伤(由酶或放射性标记铬的泄漏确定)， 产生羟基自由基(通过自旋捕捉检测到)，以及 心肌过氧化脂质的出现(通过直接测量)将 下定决心。通过铁降低铁的有效性的影响 螯合作用，细胞内pH的改变或下调 转铁蛋白受体对心肌损伤的作用将被研究。药效 活性氧代谢物的高渗透性清除剂膜 保护剂和输注巯基供体预防 心肌损伤，抑制脂质过氧化，避免衰竭 将在培养的心肌细胞中检测，分离 心脏或完整的犬类模型暴露于潜在的氧化剂损伤。

The mechanism of iron-mediated myocardial injury by reactive oxygen metabolites will be studied in cultured cardiac myocytes, isolated rabbit hearts and intact dogs. Cultured myocytes will be exposed to oxygen metabolites or activated neutrophils and the time course of membrane injury (determined by leakage of enzymes or radiolabeled chromium), production of hydroxyl radical (detected by spin trapping), and appearance of myocardial lipid peroxides (by direct measurement) will be determined. The effect of reduced iron availability through iron chelation, alterations in intracellular pH or downregulation of transferrin receptors on myocardial injury will be studied. The efficacy of highly permeable scavengers of reactive oxygen metabolites, membrane protective agents, and infusion of a sulfhydryl donor in preventing myocardial injury, inhibiting lipid peroxidation, and avoiding depletion of sulfhydryl groups will be examined in cultured myocytes, isolated hearts or intact canine models exposed to potential oxidant injury.