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目的 研究选择性诱导型一氧化氮合酶 (iNOS)抑制剂氨基胍对脑缺血 -再灌流损伤时脑微血管通透性的作用。方法 通过缺血 6 0min ,再灌流 6 0min ,造成缺血 -再灌流 (I/R)损伤 ,并制成脑窗模型 ,观察氨基胍对脑微循环通透性的影响。结果 脑缺血 -再灌流损伤后脑微循环通透性明显升高 ,并在 110s后血管外荧光物质浓度就显著高于血管内。而运用氨基胍后 ,在 80s后血管外的荧光物质浓度就显著高于血管内。结论 I/R后脑微循环通透性升高 ,iNOS激活产生的少量NO在I/R早期可能具有维持微血管通透性的作用
Objective To investigate the effect of selective inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine on cerebral microvascular permeability during cerebral ischemia-reperfusion injury. Methods The ischemic - reperfusion (I / R) injury was induced by 60 min of ischemia and 60 min of reperfusion, and the model of cerebral window was made to observe the effect of aminoguanidine on cerebral microcirculation permeability. Results The permeability of brain microcirculation was significantly increased after cerebral ischemia-reperfusion injury, and the concentration of extravascular fluorescent substance was significantly higher than that of intravascular after 110s. The use of aminoguanidine, extravascular after 80s fluorescent substance concentration was significantly higher than the intravascular. Conclusions I / R posterior cerebral microcirculation increased permeability and a small amount of NO produced by iNOS activation may have the effect of maintaining microvascular permeability in the early stage of I / R