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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
Objective To investigate the mechanism of flunarizine hydrochloride in protecting neurons after ischemia-reperfusion. Methods The gerbil model of global cerebral ischemia / reperfusion was established and randomly divided into cerebral ischemia group, flunarizine preconditioning group and control group. The mitochondria of forebrain were isolated at 1h, 6h, 1d after operation, respectively, and detected by spectrophotometry Mitochondrial permeability transition and mitochondrial free Ca2 + content. Results (1) The mitochondrial free Ca2 + concentration in forebrain was higher than that of flunarizine pretreatment and control group (P <0.01 or P <0.05) at 1 h, 6 h and 1 d after ischemia / reperfusion, (2) The mitochondrial permeability transition of forebrain at 1h, 6h, 1d after ischemia-reperfusion was more than that in control group and flunarizine pretreatment group (P <0.05). (3) In the flunarizine preconditioning group, the mitochondrial permeability transition degree of forebrain decreased most significantly at 6h after ischemia-reperfusion (P <0.01). Conclusion Flunarizine can inhibit the mitochondrial permeability transition induced by acute cerebral ischemia-reperfusion