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目的和方法：在局部脑缺血再灌注大鼠模型上，于单纯缺血２ｈ及再灌３ｍｉｎ、２ｈ、４ｈ，分离脑线粒体，检测其内ＮＯ的生成以及ＮＯ合酶（ＮＯＳ）活性的变化。结果：脑缺血时线粒体呼吸控制率（ＲＣＲ）显著下降，再灌 ４ｈ稍有恢复。与此相对应，脑线粒体 ＮＯ生成显著增加，再灌后随时间逐渐减少，４ｈ接近正常对照水平；脑缺血显著增加了脑线粒体总ＮＯＳ活性，再灌后逐渐减弱，在所观察的时间范围内，仍显著高于对照水平，而ｉＮＯＳ活性无明显变化，总ＮＯＳ活性变化主要取决于ｃＮＯＳ活性的改变。结论：脑缺血再灌过程中，脑线粒体中ＮＯＳ／ＮＯ系统激活可能参与了脑组织缺血再灌注损伤。
PURPOSE AND METHODS: Mitochondria were isolated from rat models of focal cerebral ischemia-reperfusion for 2 h and 3 min, 2 h, and 4 h after reperfusion, and the changes of NO production and NO synthase (NOS) activity were detected . Results: Mitochondrial respiration rate (RCR) decreased significantly after cerebral ischemia and recovered slightly after 4h reperfusion. Correspondingly, NO production in brain mitochondria increased significantly, and then gradually decreased with time after reperfusion, reaching to normal control level at 4 hours. Cerebral ischemia significantly increased total mitochondrial NOS activity in brain and gradually decreased after reperfusion. During the observed time range But still significantly higher than the control level, while iNOS activity did not change significantly. The change of total NOS activity mainly depends on the change of cNOS activity. Conclusion: Activation of NOS / NO system in brain mitochondria may play a role in cerebral ischemia-reperfusion injury during cerebral ischemia / reperfusion.