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研究脑反复缺血再灌流羟自由基活性动态变化，探讨脑缺血损伤的病理生理机制。方法采用Ｐｕｌｓｉｎｅｌｌｉ和Ｂｒｉｅｆｌｅｙ４血管关闭方法，５ｍｉｎ×３次缺血，用微透析针植人右侧海马ＣＡ１区，用水杨酸盐捕获生成稳定的加合物２，３和２，５二氧苯甲酸（２，３和２，５ＤＨＢＡ）。用高压液相（ＨＰＬＣ）电化学检测。结果腹腔内注射水杨酸盐和微管透析针内注射水杨酸盐，２，３和２，５ＤＨＢＡ出现相似变化。缺血期２，３和２，５ＤＨＢＡ稍降低，灌流２０ｍｉｎ显著增高，灌流１ｈ升高至顶峰，持续３ｈ。证明脑反复缺血后再灌流羟自由基显著增高，并且不是一个暂时的现象。结论自由基在脑缺血损害中起重要作用。
To study the dynamic changes of hydroxyl radical activity after repeated cerebral ischemia and reperfusion, and to explore the pathophysiological mechanism of cerebral ischemia. Methods Pulsinelli and Briefley4 were used to occlude the blood vessels. After 5min × 3 ischemia, the microdialysis needle was implanted into the right hippocampal CA1 region. Salicylate was used to capture the stable adducts 2,3 and 2,5-dioxybenzoic acid (2,3 and 2,5 DHBA). High-pressure liquid chromatography (HPLC) electrochemical detection. Results Intraperitoneal injection of salicylate and microtubule dialysis resulted in a salicylate injection, with similar changes in 2,3 and 2,5DHBA. 2, 3 and 2, 5DHBA decreased slightly in ischemic stage, perfusion 20min significantly increased, 1h perfusion increased to the peak for 3h. Proved that after repeated cerebral ischemia and reperfusion of hydroxyl free radicals was significantly increased, and is not a temporary phenomenon. Conclusion Free radicals play an important role in cerebral ischemia.