Werns S W, Lucchesi B R
Department of Internal Medicine (Division of Cardiology), University of Michigan Medical School, Ann Arbor 48109.
Free Radic Biol Med. 1988;4(1):31-7. doi: 10.1016/0891-5849(88)90008-1.
Ischemic myocardium generates stimuli for neutrophil chemotaxis before the final extent of irreversible ischemic injury is attained. Reperfusion accelerates the infiltration of ischemic myocardium by neutrophils. Oxygen radicals released by the activated neutrophils may exacerbate the tissue damage caused by ischemia. Neutrophil depletion by antiserum was shown to limit infarct size in dogs undergoing coronary occlusion for 90 minutes followed by reperfusion for 6 or 72 hours, but not in dogs undergoing occlusion for 4 hours. Prostacyclin, which inhibits the generation of superoxide anions by neutrophils, also limited canine myocardial injury despite no effect on collateral blood flow. Iloprost, an analogue of prostacyclin that inhibits neutrophils also reduced infarct size, while SC39902, an analogue that does not inhibit neutrophils, did not alter infarct size. The results suggest that oxygen radicals released by activated neutrophils play a role in the pathophysiology of myocardial injury due to ischemia followed by reperfusion.
在达到不可逆性缺血损伤的最终程度之前，缺血心肌会产生刺激中性粒细胞趋化的因子。再灌注会加速中性粒细胞对缺血心肌的浸润。活化的中性粒细胞释放的氧自由基可能会加剧缺血所致的组织损伤。抗血清清除中性粒细胞可使冠状动脉闭塞90分钟后再灌注6或72小时的犬梗死面积减小，但对冠状动脉闭塞4小时的犬则无此作用。前列环素可抑制中性粒细胞超氧阴离子的生成，尽管其对侧支血流无影响，但也能限制犬心肌损伤。伊洛前列素是一种抑制中性粒细胞的前列环素类似物，它也能减小梗死面积，而不抑制中性粒细胞的类似物SC39902则不会改变梗死面积。这些结果表明，活化的中性粒细胞释放的氧自由基在缺血后再灌注所致心肌损伤的病理生理过程中起作用。
