大鼠局灶性脑缺血/再灌注后脑微血管中NO含量的动态变化

目的:探讨局灶性脑缺血/再灌注不同时相脑微血管及某些脑区中NO含量变化,为临床应用NO合酶抑制剂提供实验依据。方法:将Wister大鼠随机分为假手术（S）、缺血（I）和再灌注（R）3大组。采用线栓法造成大鼠右侧大脑中动脉阻塞的局灶性脑缺血/再灌注模型。以蛋白漂洗法提取大鼠右侧大脑皮层的脑微血管,Lowry法测定蛋白含量。荧光分光光度法测定NO含量。结果:脑缺血不同时相脑微血管中NO含量呈渐进性升高（I1、I4、I8组与S组比较,P<0.01）,I24组虽较S组略有升高,但无统计学差异;在纹状体与海马,除I1与I8外,其余各组均显著下降（P<0.01）;再灌注不同时相脑微血管中除I1R23组显著升高（P<0.01）外,其余两组无明显变化;在脑区,无论纹状体与海马,均显著下降（P<0.01）。结论:在局灶性脑缺血/再灌注不同时相、不同部位,其NO含量变化不同,提示NO参与局灶性脑缺血/再灌注的病理生理过程。

The dynmnic change of nitric oxide of brain microvessel after focal cerebral ischemia/reperfusion in rats

Objective:To study the change of nitrogen monoxide(NO) content in difference phase of brain microvessel and areas during focal cerebral ischemia/reperfusion in rats for broadening treatment way by applying inhibitor of NO synthase. Methods: Wister rats were divided randomly into three groups: sham(S) ,ischemia(I)and reperfusion(R). The rat right focal cerebral ischemia/reperfusion model was made by blocking the MCA with thread. The brain microvessel of the right cortex was isolated by protein floated. The protein contents were measured by Lowry's method. The NO contents were determined by fluorescence spectrophotometer. Results:The experiments showed that NO contents of the brain microvessel were increased progressively compared with that of the sham group( I1, I4 and I8, P<0.01)in the different phase of cerebral ischemia, I24 group was increased slightly but no statistical difference was seen. Except I1 and I8 groups, NO contents of other groups were decreased signinificantly compared with that of S group(P<0.01)in the striatum and hippocampus. In the different phase of the reperfusion,significant increased was seen(P<0.01)only in I1R23 group . Statistical difference was not seen in the other group of the brain microvessel. In the cerebral areas,NO contents of the striatum and hippocampus were both decreased(P<0.01).Conclusion:In the differcent phase and cerebral areas of the focal cerebral ischemia/reperfusion, NO content changes were different . The results suggested that the NO participates in pathophysiological course of the focal cerebral ischemia/reperfusion.