通常认为缺血心肌“再灌注”时心肌细胞黄嘌呤氧化酶系统产生了大量的氧自由基(oxygen freeradical OFR),并由此造成组织脂质过氧化损伤。近年研究发现人类及兔心肌该酶系活性极低,提示存在产生OFR的其它途径。晚近观察到有大量的白细胞(尤为中性粒细胞neutrophil,Neu)浸润至缺血心肌,并加重心肌损伤,因此本文对Neu功能与脂质过氧化损伤进行了相关性研究。 It is generally believed that the cardiomyocyte xanthine oxidase system produces a large amount of oxygen free radical OFR during “reperfusion” of the ischemic myocardium and thereby causes tissue lipid peroxidation damage. Recent studies have found that human and rabbit myocardial enzyme activity is very low, suggesting that there are other ways to produce OFR. We recently observed a large number of leukocytes (especially neutrophil, Neu) infiltrated into the ischemic myocardium, and aggravate myocardial injury, so this article Neu function and lipid peroxidation damage were studied.