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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。
Objective: To investigate the relationship between the changes of nitric oxide synthase (NOS) and the apoptosis of brain cells during focal cerebral ischemia-reperfusion, and to explore the time window of blocking the apoptosis of brain cells. Methods: The focal cerebral ischemia model was established by thread occlusion. The MCAO time was 15, 30, 60, 90, 120 min and reperfusion for 24 h. The NOS activity in the ischemic center (parietal cortex and caudate putamen) after focal cerebral ischemia / reperfusion was detected by using the reduced NADPH-d histochemical method. Hematoxylin and eosin and TUNEL staining were used to detect the apoptosis of brain cells in the ischemic center. Results: The number of NOS-positive neurons increased most significantly at 30 min and sharply decreased at 90-120 min. The number of apoptotic cells in each group increased with prolonged ischemia. Conclusion: Neuronal NOS (nNOS) plays a major role in the early stage of ischemic brain injury, especially apoptosis in focal cerebral ischemia / reperfusion.