沙土鼠脑缺血再灌注诱导线粒体通透性转换和氟桂嗪的影响

目的　进一步探讨盐酸氟桂嗪对缺血再灌注后神经细胞保护作用的机制。方法　制作沙土鼠全脑缺血 /再灌注模型 ,随机分为脑缺血组、氟桂嗪预处理组和对照组 ,分别于术后 1h、6h、1d分离前脑线粒体 ,用分光光度法检测线粒体通透性转换以及线粒体游离Ca2 + 的含量。结果　 (1)前脑线粒体游离Ca2 +浓度在缺血再灌注后 1h、6h、1d均高于氟桂嗪预处理和对照组 (P <0 .0 1或P <0 .0 5 ) ,以缺血再灌注后 6h最明显 (P <0 .0 1) ;(2 )缺血再灌注后 1h、6h、1d前脑线粒体通透性转换开放程度较对照组和氟桂嗪预处理组均高 (P <0 .0 5 ) ;(3)氟桂嗪预处理组以缺血再灌注后 6h前脑线粒体通透性转换开放程度降低最为显著(P <0 .0 1)。结论　氟桂嗪抑制急性脑缺血再灌注诱导的线粒体通透性转换

Mitochondrial Permeability Transition induced in gerbil brain after ischemia reperfusion and the effection of flunarizine

Objective To investigate the protective mechanism of flunarizine in gerbil brain after ischemia reperfusion.Methods Gerbils with brain ischemia and reperfusion were assigned into two groups:group with and without flunarizine pre treated, and normal group was also set. Mitochondrial were extracted from fore head on 1h, 6h and 1d after operation respectively. Mitochondria permeability transition and free Ca 2+ concentration were measured by spectrophotometer.Results The concentration of Ca 2+ in fore head mitochondria after brain ischemia reperfusion were higher than other groups( P < 0.01 or P < 0.05 ) in which the group of 6h after operation was the most remarkable. The mitochondria permeability transitions were more opened in ischemia group than the others ( P < 0.05 );in flunarizine pre treated group, the mitochodial permeability transition was obviously less opened in group of 6h after operation ( P < 0.01 ).Conclusions Flunarizine inhibit the opening of gerbil fore head mitochondria permeability transition induced by acute brain ischemia/reperfusion.