大鼠全脑缺血再灌注后脑组织一氧化氮合酶的变化

目的 观察全脑缺血再灌注后神经元型一氧化氮合酶(neuronal nitric oxide synthese，nNOS)与诱导型一氧化氮合酶(inducible nitric oxide synthase，iNOS)的变化，从而探讨一氧化氮在脑缺血再灌注损伤中的作用。方法 实验分为正常组、假手术组、缺血组，采用大鼠4血管夹闭方法制作全脑缺血再灌注模型，观察nNOS、iNOS在缺血20min再灌注2h、6h、1d、3d、5d、7d时的变化及大脑皮层、海马、丘脑的组织病理学改变。结果 nNOS在缺血再灌注后2h开始升高，1d达高峰，3d开始下降，iNOS在再灌注2h开始表达，3d达高峰，5d开始下降，并持续至7d。结论 脑缺血再灌流时nNOS和iNOS表达增强，尤其是iNOS在灌注后期表达，提示N0生成增多可能与缺血后迟发性神经元死亡有关。

The alterations of nitric oxide in brain during reperfusion after global cerebral ischemia in rats

Objective To investigate the role of nitric oxide (NO) in ischemia reperfusion (I/R) injury by observing the alterations of neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) during reperfusion after global cerebral ischemia in rats.Methods Adult male Wistar rats were randomly divided into three groups: normal group, control group and ischemic group. Global ischemic model was established by 4 vessel occlusion. The rats were killed at 2h, 6h, 1d, 3d, 5d, 7d,respectively,after 20 mins of ischemia. Immunohistochemical method and light microscope were used to observe the alterations of nNOS, iNOS and histopathological changes in brain cortex, hippocampi, and thalamus at above mentioned time points respectively. Results nNOS tented to increase at 2h, reached peak level at 1d and decreased at 3d, iNOS began to express at 2h, reached peak level at 3d, reduced at 5d and lasted till 7d.Conclusion The expression of nNOS and iNOS increase in ischemia reperfusion,and iNOS expresses significantly in late period of reperfusion, which suggests the increase of NO may be related to the delayed neuronal death after ischemia.