摘要
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 。
Objective To evaluate the effect of diazepam on concentration of aminoacids in rat cortex during cerebral ischemia and reperfusion. Methods Sixty three Wistar rats were divided randomly into nine groups: control group( n =7), ischemia groups-is 3 h, is 3 h/rep 1 h, is3 h/rep 2 h, is3 h/rep 3 h(each group, n =7),diazepam treatment groups (10 mg/kg i.p.)-is 3 h, is 3 h/rep 1 h, is3 h/rep 2 h, is 3 h/rep 3 h(each group, n =7)with revised Zivin JV's animal nodel of middle cerebral artery occlusion.Results Compared with ischemia groups,we find that glutamate and aspartate decreased markedly and GABA increased markedly in treatment groups.Conclusion It indicates that diazepam can influence the synthesis and release of excitotary/inhibitory amino acids.
出处
《卒中与神经疾病》
2001年第3期147-149,共3页
Stroke and Nervous Diseases
关键词
地西泮
兴奋性/抑制性氨基酸
缺血再灌注
Diazepam Excitotary/Inhibitory animo acids Ischemia and reperfusion