摘要
目的:本实验通过观察大鼠局灶性脑缺血-再灌注后脑组织一氧化氮(NO)水平的变化以及苯妥英(PHT)对其影响,以进一步探讨局灶性脑缺血-再灌注损伤机制及PHT对缺血-再灌注损伤后保护作用的机制。方法:将雄性成年Wistar大鼠随机分为4组:即假手术组、缺血-再灌注组、PHT低剂量治疗组和PHT高剂量治疗组。每组均观察手术后6h、12h、24h三个时间点的改变。采用线栓法制成大脑中动脉闭塞模型。测定手术后不同时点缺血脑组织NO的水平。结果:缺血-再灌注组各时点NO水平与假手术组相应时点比较明显升高,具有显著性差异(P<0.05),PHT低剂量治疗组和高剂量治疗组NO水平明显低于缺血-再灌注组各相应时间点(P<0.05),PHT高剂量治疗组各时点NO水平与PHT低剂量治疗组各相应时间点比较明显降低(P<0.05)。结论:脑缺血-再灌注后,缺血大鼠脑组织内的NO水平升高,说明NO参与了脑缺血-再灌注损伤的病理生理过程;PHT可降低NO水平,从而对脑缺血-再灌注损伤可能具有保护作用。
Objective： To explore the protective effect of phenytoin on experimental cerebral ischemia-reperfusion injury of rats and the possible mechanism. Methods： The model of focal brain ischemia was prod-uced by an intralumin al suture occulusion of the middle cerebral artery （ MCA ） in rats. 60 adult male wistar rats were used. The rats were randomly divided into four groups： sham operation group undergoing all surgical procedures but the intraluminal suture occulusion of the middle cerebral artery, ischemia-reperfusion group, two treatment groups （phenytion at 20mg/kg, 40mg/kg）. Every group was divided into 3 various stages： post operation 6h, 12h, 24h. The level of nitric oxide （NO） was analyzed by spectrophotometry. Results; The level of NO at various stage in ischemiareperfusion group were higher than those in sham operation group （P 〈0.05 ）. Those of NO at various stages in phenytion （20mg/kg, 40mg/kg, ip）treatment groups were lower than those in ischemia- reperfusion group （P 〈0. 05）. The levels of NO at various stages in phenytion （40mg/kg, ip）treatment group were lower than those in phenytion （20mg/kg, ip） treatment group （P 〈0.05）. Conclusion： The levels of NO of rats in ischemia-reperfusion group were notably increased. It showed that NO played a role in the physicological functions of ischemia-reperfusion injury. Phenytion reduced the levels of NO.
出处
《陕西医学杂志》
CAS
北大核心
2007年第8期952-954,共3页
Shaanxi Medical Journal
关键词
脑缺血/并发症
再灌注损伤
一氧化氮
苯妥英
Brain ischemia/complications Reperfusion injury Nitric oxide Phenytoin
