摘要
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。
Objective To obtain direct evidence of oxygen radical activily, study on pothogenisis ofcerebral ischemia. Methods We used chemical tripping of hydroxyl radical in the form of the stableadducts 2, 3- and 2, 5-dihydroxybenzoic acid (DHBA) following salicylate administration. Wistar ratswere subjected to 5min×3 of global forebrain ischemia by 4VO, salicylatc was administered either systemically (200mg/kg,i. p. )or by continous infusion (5mM) through a microdialysis probe implanted inthe hippocompus. DHBA were assayed by HPLC with electrochemical detection. Results Followingsystemic administration of salicylate, stable bascline levels of HDBA were obeserved before ischemia aslightly reduction in mean levels of both DHBA was ducumented during ischemia. During recirculation,DHBA levels increased. It was peak for 1h. The increase in DHBA levels persisted for 3h. ConclusionThese results provide evidence that hydroxyl radical levels are increased during postichomic recirculation.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
1999年第1期12-14,共3页
Journal of Apoplexy and Nervous Diseases
基金
河北省科委重点资助项目!No94216101D
关键词
脑缺血
自由基活性
透析
海马
再灌注损伤
Cerebral ischemia Hydroxyl radical Microdialysis Hippocampus
