苯妥英对局灶性脑缺血——再灌注后脑组织自由基含量的影响

目的观察大鼠局灶性脑缺血-再灌注后脑组织自由基的变化及苯妥英（PHT）对其改善的影响．并探讨其保护作用机制。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。采用线栓法制成大脑中动脉闭塞模型，每组均于手术后6h、12h、24h三个时间点测定脑组织超氧化物歧化酶（SOD）活力和丙二醛（MDA）水平的改变。结果缺血-再灌注组各时点SOD活力显著低于假手术组相应时点SOD活力（P〈0．05），PHT低剂量治疗组和高剂量治疗组SOD活力明显高于缺血-再灌注组各时点SOD活力（P〈0.05），PHT高剂量治疗组各时点SOD活力又明显高于低剂量治疗组，且具有显著性差异（P〈0．05）；缺血-再灌注组MDA水平显著高于假手术组相应时点MDA水平（P〈0.05），PHT低剂量治疗组和高剂量治疗组MDA水平与缺血-再灌注组各相应时间点比较明显降低（P〈0．05），PHT高剂量治疗组MDA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MDA的水平升高，SOD活力降低，说明自由基参与了脑缺血-再灌注损伤的病理生理过程。PHT可降低MDA的水平，增加SOD的活性，从而对脑缺血-再灌注损伤具有保护作用。

Experimental research of protective effect of phenytoin in cerebral ischemia-reperfusion injury of rats

Objective To explore the protective effect of phenytoin on experimental cerebral ischemia-reperfusion injury of rats and its possible mechanism. Methods The model of focal brain ischemia was made by an intraluminal suture occulusion of the middle cerebral artery ( MCA ) in adult male wistar rats. 60 rats were randomly divided into four groups:sham-operation group, ischemia-reperfusion group and two treatment groups (phenytion 20mg/kg or 40mg/kg). After operation 6h,12h, 24h.the activities of SOD and the concentration of MDA were measured in every group. Results The activities of SOD in ischemia-reperfusion group were lower than those in sham-operation group (P<0.05) at various stages,but in phenytion (20mg/kg,40mg/kg,i) treatment groups were higher than those in ischemia-reperfusion group (P<0.05) and the 40mg/kg phenytion group was higher than those in 20mg/kg phenytion group (P<0.05). The concentrations of MDA in ischemia-reperfusion group at various stage were higher than those in sham-operation group ( P<0.05 ),and in 40mg/kg phenytion groups were lower than those in (P<0.05), but in phenytion (20mg/kg,40mg/kg) treatment group were lower than those in ischemia-reperfusion group. Conclusion The elevation of MDA levels. and the lovering of SOD activety might take part in the ischemia-reperfusion injury. and phenytion could have the effect of decrease the levels of MDA and increase the activities of SOD.