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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)活性变化与脑缺血损伤的关系 ,探索脑缺血的治疗时间窗。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、6 0、90、12 0min ,再灌注 2 4h。用NADPH d组织化学法 ,检测局灶性脑缺血再灌注后缺血半暗区和中心区NOS活性变化。结果 :半暗区NOS阳性神经元数量于 6 0min达峰值 ;中心区NOS阳性神经元数量于 30min达峰值 ,90～ 12 0min急剧减少。结论 :局灶性脑缺血再灌注过程中NOS参与脑缺血损伤 ,在中心区与半暗区NOS活性变化不一致 ,半暗区NOS达峰值时间较中心区延长。推测中心区运用NOS抑制剂最佳时机在 30min内 ,半暗区最佳时机在 6 0min内
Objective: To investigate the relationship between the changes of nitric oxide synthase (NOS) activity and cerebral ischemic injury during focal cerebral ischemia-reperfusion and explore the therapeutic window of cerebral ischemia. Methods: The model of focal cerebral ischemia was established by thread occlusion. The MCAO occlusion time was 15, 30, 60, 90, 120 min and reperfusion 24h. NADPH d histochemical method was used to detect the changes of NOS activity in the penumbra and center after focal cerebral ischemia and reperfusion. Results: The number of NOS positive neurons in the penumbra reached a peak at 60 min. The number of NOS positive neurons in the central area peaked at 30 min and sharply decreased from 90 min to 120 min. CONCLUSION: NOS participates in cerebral ischemic injury during focal cerebral ischemia / reperfusion, and there is inconsistent change of NOS activity in central and semi-dark area. NOS peak time in semi-dark area is longer than central area. It is speculated that the best time to use NOS inhibitors in the central area within 30min, the best time in the dark area within 60min