【摘要】 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。更多还原

【Abstract】 AIM and METHOD:To determine the production of nitric oxide(NO) and change of NO synthase(NOS) activity in mitochondria isolated from the rat brains of the ischemia/reperfusion rat model produced by transient occlusion of middle cerebral artery on the following the points: 2 h after occlusion of artery and 30 min, 2h, 4h after reperfusion. RESULTS: After the occlusion of middle cerebral artery, the respiratory control rate(RCR) of mitochondria significantly decreased and slightly increased at 4h after reperfusion. Meantime, the production of NO in mitochondria increased significantly. But with the increase of perfusion, production of NO gradually decreased and reached normal level as in the control group. It also shows that cerebral ischemia increased NOS’s activity significantly in the mitochondria and still kept a higher level than the control group although it decreased gradually after reperfusion. But the iNOS’s activity did not show obvious change. The change of total NOS’s activity depends on the change of cNOS’s activity. CONCLUSION: The activation of NO/NOS system in the mitochondria might play an important role in the reperfusion injury during reperfusion of ischemic brain.更多还原