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作 者:梅世昌[1] 白林 陈卫东[2] 许潇[3] 谢林[3] 刘晓东[3]
机构地区:[1]解放军总医院,北京100853 [2]马鞍山十七冶医院,安徽马鞍山243000 [3]中国药科大学药代研究中心,江苏南京210009 [4]不详
出 处:《解放军药学学报》2009年第2期159-161,共3页Pharmaceutical Journal of Chinese People's Liberation Army
摘 要:目的研究脑缺血再灌损伤是否影响银杏内酯B在脑内处置。方法大鼠大脑中动脉阻断缺血2h,再灌10min后,静脉注射12mg.kg-1银杏内酯B,于给药后不同时间处死动物,分取用LC/MS方法测定血浆、缺血侧和对照侧脑组织中银杏内酯B浓度。结果缺血侧脑组织中银杏内酯B浓度显著高于对照侧,其AUC约为对照侧的1.88倍。与正常动物比较,脑缺血鼠的血药浓度显著低于正常大鼠,其AUC仅为正常鼠的1/3。结论脑缺血损伤可改变银杏内酯B体内药代动力学行为,增加脑内浓度。Aim To study whether brain ischemia/reperfusion affects pharmacokinetics of ginkgolide B in rats. Methods Brain ischemia was induced by middle cerebral artery occlusion for 2 h, followed by 10 min reperfusion. A dose of 12mg·kg^-1 ginkgolide B was intravenously given to the rats that were sacrificed at a designed time. Blood, ipsilateral and contralateral cerebral samples were obtained. The concentrations of ginkgolide B in plasma, ipsilateral and controlateral cerebral tissues were measured using LC/MS method. Results Concentrations of ginkgolide B in ipsilateral cerebral tissues were significantly higher than those in contralateral cerebral tissue, and the value of AUC in contralateral tissue was 1.88-fold that in contralateral tissue. The plasma concentrations of ginkgolide B were significantly lower than those in normal rats and the value of AUC was only one third that of normal rats. Conclusion Brain damage induced by middle cerebral artery occlusion/reperfusion may change pharmacokinetic behaviour of ginkgolide B in rats.
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