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目的 探讨外源性血小板激活因子 (PAF)激活的多核形中性粒细胞 (PMN)是否具有低浓度氧自由基模拟缺血预适应 (IP)对缺血再灌注 (IR)所致心肌损伤的保护作用。方法 结扎冠脉左前降支 30min ,再灌注 3h制备大鼠心脏IR模型。以缺血前给予 2次 5min缺血 ,10min再灌注作为IP。实验分为6组 ,IR组、IR +PAF组和IR +银杏内酯B(GB、PAF拮抗剂 )组 ,分别于缺血前 2 5和 10miniv生理盐水、PAF(3μg·kg- 1)和GB (5mg·kg- 1) ;IP +IR组、IP +IR +PAF组和IP +IR +GB组分别于IP 2次 10min再灌注开始时iv相应药物。观察分析心功能、梗死面积、PMN计数、心肌髓过氧化物酶活性、TUNEL阳性细胞计数等指标。结果 给予PAF明显加重IR引起的心脏损伤、PMN浸润及凋亡的程度 ;GB对IR引起的心功能下降没有明显影响 ,但明显减少梗死面积、PMN浸润及凋亡细胞 ;PAF明显削弱IP的保护作用 ;GB对IP作用未见明显影响。结论 IR后PMN浸润可能是引起心肌细胞凋亡的一个重要原因 ;PAF激活PMN可能不具有模拟IP对IR所致心肌损伤的保护作用 ,反而取消IP的保护作用。
Objective To investigate whether polymorphonuclear neutrophils (PMN) activated by exogenous platelet activating factor (PAF) have the effect of hypoxia-ischemia preconditioning (IP) on myocardial injury induced by ischemia-reperfusion (IR) Protective effects. Methods The left anterior descending coronary artery was ligated for 30 minutes and then reperfused for 3 hours to prepare rat heart IR model. 2 min before ischemia to give 5min ischemia, 10min reperfusion as IP. The rats were divided into 6 groups: IR group, IR + PAF group and IR + Ginkgolide B group (GB, PAF antagonist) GB (5mg · kg-1). The IP + IR group, the IP + IR + PAF group and the IP + IR + GB group were iv treated with corresponding drugs at the beginning of 10 min IP 2 reperfusion. Observation and analysis of cardiac function, infarct size, PMN count, myocardial myeloperoxidase activity, TUNEL positive cell count and other indicators. The results showed that PAF significantly increased the degree of cardiac damage, PMN infiltration and apoptosis induced by IR. GB had no significant effect on the decrease of cardiac function induced by IR, but significantly reduced infarct size, PMN infiltration and apoptotic cells; PAF significantly weakened the protection of IP Role; GB on the role of IP no significant effect. Conclusions PMN infiltration may be one of the important causes of cardiomyocyte apoptosis after IR. Activation of PMN by PAF may not have the protective effect of simulating IP on myocardial injury induced by IR, but may reverse the protective effect of IP.