脑缺血再灌注大鼠脑线粒体NO的生成及NOS活性的改变.docVIP

???? 脑缺血再灌注大鼠脑线粒体NO的生成及NOS活性的改变 ???? ????［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2 h及再灌30 min、2 h、4 h，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4 h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，4 h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。　　［主题词］　脑；局部缺血；再灌注损伤；线粒体；一氧化氮；大鼠　　［中分类号］　Q463　　［文献标识码］　A　　［文章编号］　1000-4718(2000)04-0289-04 Production of nitric oxide and change of nitric oxide synthase activity in brains mitochondria of the rats with focal cerebral ischemia/reperfusion WANG-Lei, XU Jian-xing, TANG Chao-shu, CHEN Qing-tang(Center of Neurology Research and Institute of Cardiovascular Research, First Clinical Hospital,Beijing Medical University, Beijing 100083，China) 　　［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 time points:2 h after occlusion of artery and 30 min,2 h, 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 NOSs activity significantly in the mitochondria and still kept a higher level than the control group although it decreased gradually after reperfusion.But the iNOSs activity did not show obvious change.The change of total NOSs activity depends on the change of cNOSs 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.　　［MeSH］　Brain；Ischemia；R