局灶性脑缺血预处理对大鼠脑缺血再灌注损伤的保护作用及其机制

目的:探讨局灶性脑缺血预处理在大鼠脑缺血再灌注损伤中的作用及其与一氧化氮(NO)的关系.方法:线栓法制作大鼠大脑中动脉阻塞的局灶性脑缺血模型.在此模型上,脑缺血预处理10 min再灌注72 h后,再次脑缺血90 min后再予再灌注24 h,用Bederson神经缺损体征评分法评估大鼠神经功能缺损,用亚硝酸盐还原法测定脑组织中NO的含量.结果:脑缺血90 min再灌注24 h后,脑缺血预处理 脑缺血再灌注组(IP R组)大鼠的神经功能缺损体征明显轻于假脑缺血预处理 脑缺血再灌注组(R组)(P＜0.05);R组和IP R组的缺血侧和自身对照侧皮层、海马的NO含量异常升高,与假脑缺血预处理 假脑缺血再灌注组(S组)相比差异均有统计学意义(P＜0.01);IP R组缺血侧和自身对照侧皮层、海马的NO含量较R组明显下降,差异有统计学意义(P＜0.01).结论:脑缺血预处理对大鼠脑缺血再灌注损伤具有保护作用,其机制可能是降低了脑组织的NO水平.

THE PROTECTIVE EFFECT OF FOCAL CEREBRAL ISCHEMIC PRECONDITION ON CEREBRAL ISCHEMIA-REPERFUSION INJURY AND ITS MECHANISM IN RATS

Objective: To investigate the effect of focal cerebral ischemic precondition on cerebral ischemia-reperfusion injury in rats and the link between the effect and cerebral nitric oxide (NO).Methods: The middle cerebral artery occlusion (MCAO) model of rat was made by using a thread to occlude the right middle cerebral artery. By this MCAO model, first, cerebral ischemic precondition 10 min and reperfusion 72 h, and then cerebral ischemia 90 min and reperfusion 24 h again. The neurologic function wane of rats was estimated by Bederson method. The cerebral content of NO was measured by nitrite reduction. Result: After 90 min cerebral ischemia and 24 h ischemia-reperfusi-on, the neurologic disorders of the cerebral ischemia-reperfusion with ischemic precondition group (IP+R group) of rats were less severe significantly than those of the ischemia-reperfusion with sham ischemic precondition group (R group) rats (P<0.05); the content of NO in cerebral cortex and hippocampal region of the ischemic and self-control side of R group and IP+R group rats were significantly more than that of the sham ischemia-reperfusion with sham ischemic precondition group (S group)of rats (P<0.01); the content of NO in cerebral cortex and hippocampal region of the ischemic side and self-control side of the IP+R group of rats were significantly less than those of the R group of rats (P<0.01).Conclusion: Cerebral ischemic precondition may have protection against cerebral ischemia-reperfusion injury of rats. The neuroprotective mechanism of cerebral ischemic precondition may reduce the cerebral content of NO in rats.