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目的 评价双苯氟嗪 (Dip)和氟桂利嗪 (Flu)在大鼠局灶性脑缺血再灌注模型中的神经保护作用。方法 将内皮素 1(ET 1)灌注到大脑中动脉附近制备大鼠局灶性脑缺血再灌注模型 ,并于灌注ET 1后 30min和 4 .5h腹腔注射溶剂、Dip 10 ,2 0和4 0mg·kg- 1和Flu 2 0mg·kg- 1,采用氢清除法监测灌注ET 1前、后纹状体血流变化 ,并对缺血后 2 4h脑梗塞面积、血清中超氧化物歧化酶 (SOD)活性和丙二醛 (MDA)含量的变化进行了测定。结果 Dip 2 0和 4 0mg·kg- 1于灌注ET 1后 70和 10 0min明显改善缺血侧纹状体血流量下降 ;Flu 2 0mg·kg- 1的作用较弱 ,仅于灌注ET 1后 10 0min明显改善缺血侧纹状体血流量 ;Dip可以剂量依赖性的降低脑梗塞面积 (r =0 .9797,P <0 .0 1) ,同剂量Flu可产生相似的作用 ;各剂量组Dip和Flu均可增加血清中SOD活性、降低MDA含量。结论 Dip和Flu对脑缺血再灌注损伤有明显的保护作用 ,Dip改善脑血流的作用略强于Flu ,其保护作用的机制与改善脑血流和抗氧化作用有关。
Objective To evaluate the neuroprotective effects of Diphenhydrofolazine and Flunarizine on focal cerebral ischemia-reperfusion in rats. Methods Focal cerebral ischemia-reperfusion model was induced by perfusing endothelin 1 (ET 1) into the middle cerebral artery and intraperitoneal injection of solvents, Dip 10, 20 and 4 30 min and 4.5 h after ET 1 infusion 0 mg · kg-1 and Flu 2 0 mg · kg-1. The changes of blood flow in the striatum before and after perfusion of ET 1 were monitored by hydrogen scavenging method. The infarct size, the level of superoxide dismutase SOD activity and malondialdehyde (MDA) content were measured. Results Dip 2 0 and 40 mg · kg -1 significantly decreased the blood flow of ischemic striatum at 70 and 100 min after ET 1 infusion. The effect of Flu 2 0 mg · kg -1 was weaker and only after ET 1 infusion Dip at a dose-dependent manner reduced the area of cerebral infarction (r = 0.9797, P <0.01), and the same dose of Flu could produce a similar effect. Each dose group Dip and Flu can increase serum SOD activity, reduce MDA content. Conclusions Dip and Flu have significant protective effects on cerebral ischemia-reperfusion injury. Dip can improve cerebral blood flow slightly better than Flu, and its mechanism of protection is related to cerebral blood flow and antioxidation.