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目的 研究地西泮在脑缺血再灌注损伤中的保护作用机制。方法 将Wistar大鼠随机分为 9组 ,假手术组 7只 ,缺血组又分为缺血 3h组、缺血 3h后分别再灌注 1h、2h、3h组各 7只 ;治疗组 (即在缺血前 30分钟给予地西泮 10mg/kg ,腹腔给药 )又分为缺血 3h组、缺血 3h后分别再灌注 1h、2h、3h组各 7只。动物模型参照ZivinJA大脑中动脉线栓模型并加以改进。结果 给予地西泮后能明显减少谷氨酸(Glu)和天门冬氨酸 (Asp)的产生 ,增加r 氨基丁酸 (GABA)的生成和释放。结论 地西泮可能是通过增强抑制性氨基酸的合成和释放 ,降低兴奋性毒性来保护缺血神经元的
Objective To study the protective effect of diazepam on cerebral ischemia-reperfusion injury. Methods Wistar rats were randomly divided into 9 groups and 7 sham-operation groups. The rats in ischemia group were divided into ischemia 3h group and ischemia-reperfusion group (7h, 2h, 3h) 30 min before ischemia, diazepam 10mg / kg, intraperitoneal administration) were divided into ischemia 3h group, ischemia 3h after reperfusion 1h, 2h, 3h group 7 each. The animal model was modeled on the ZivinJA middle cerebral artery occlusion model and improved. Results After diazepam administration, the production of glutamate (Glu) and aspartate (Asp) and the production and release of r-aminobutyric acid (GABA) were significantly decreased. Conclusion Diazepam may protect ischemic neurons by enhancing the synthesis and release of inhibitory amino acids and reducing excitotoxicity