MECHANISMS OF MYOCARDIAL REPERFUSION INJURY

铁介导的活性氧心肌损伤机制 代谢物将在培养的心肌细胞、分离的兔 心脏和完整的狗 培养的肌细胞将暴露于氧气中 代谢产物或活化的中性粒细胞和时间过程的膜 损伤（通过酶或放射性标记铬的泄漏确定）， 产生羟基自由基（通过自旋捕获检测），和 心肌脂质过氧化物的出现（通过直接测量）将 测定 通过铁减少铁可用性的影响 螯合，细胞内pH值的改变或 转铁蛋白受体对心肌损伤的影响。 疗效 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， 心肌损伤，抑制脂质过氧化，避免耗竭 将在培养的肌细胞中检查巯基的含量，分离 心脏或暴露于潜在氧化剂损伤的完整犬模型。

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.