大鼠局灶性脑缺血后─氧化氮合酶活性与细胞凋亡关系

目的：了解局灶性脑缺血再灌注过程中一氧化氮合酶（ＮＯＳ　）变化与脑细胞凋亡的关系，探索阻断脑细胞凋亡的时间窗。方法：用线栓　法建立局灶性脑缺血模型，大脑中动脉阻塞（ＭＣＡＯ）的时间分别为１５、３０、６０、９０、１２０　ｍｉｎ　，再灌注２４　ｈ。用还原型尼克酰胺腺嘌呤二核苷酸脱氢酶（ＮＡＤＰＨ－ｄ）组化法，检测局灶性脑　缺血再灌注后缺血中心区（顶叶皮层和尾壳核）ＮＯＳ活性变化。用苏木精－伊红和ＴＵＮＥＬ染色法　检测缺血中心区脑细胞凋亡情况。结果：ＮＯＳ阳性神经元数于３０　ｍｉｎ时增多　最显著，９０～１２０　ｍｉｎ时急剧减少。各组凋亡细胞数随缺血时间延长而增多。结　论：局灶性脑缺血再灌注过程中神经型ＮＯＳ（ｎＮＯＳ）对缺血早期的脑损伤尤其是细胞　凋亡起主要作用。

The Relationship between Nitric Oxide Synthase Activity and Cerebral Apoptosis after Focal Cerebral Ischemia in Rats

Objective:To investigate the relationship between the variation of nitric oxide synthase activity and cerebral apoptosis during focal cerebral ischemia and reperfusion; and explore the therapeutic window by interr upting cerebral apoptosis. Methods: The middle cerebral artery of rats was occluded for 15,30,60,90 or 120 min by an intraluminal filament, and re circulation was instituted and maintained for 24 h. Nitric oxide synthase ac tivity and cerebral apoptosis in ischemic core area (parietal cortex and caudopu tamen) was examined after focal cerebral ischemia and reperfusion using NADPH-d histochemistry technique and HE or TUNEL staining method. Results: T he nitric oxide synthase activity of ischemic core area peaked at 30 min the n downregulated at 90-120 min sharply. The quantity of cerebral apoptosis i ncreased with longer ischemic period. Conclusion: The neuronal Nitric oxide synthase plays a role in early cerebral ischemic damage especially apoptos is during focal cerebral ischemia and reperfusion.