线粒体Ca^(2+)超载与缺血性脑损伤  

Mitochondria calcium overload and ischemic brain injury

作　　者：杨宾侠[1] 张煜东[1] 赵砚丽[1] 王永利[2] 

机构地区：[1]河北省人民医院麻醉科,石家庄市050071 [2]河北医科大学药理教研室,石家庄市050017

出　　处：《国际麻醉学与复苏杂志》2006年第6期365-368,共4页International Journal of Anesthesiology and Resuscitation

摘　　要：Considerable studies on molecular mechanism of brain ischemia reperfusion had been conducted in recent years,including the changes of calcium homeostasis,the gengeration of free radicals and the disorder of mitochondria function,activation of protein kinase,and the expression of gene inflammation and so on.Among them,the disorder of mitochondria function plays an important role in brain ischemia reperfusion Injury.Aiming at the change of cytoplasm,mitochondria calcium homeostasis and disorder of mitochondria function,we discuss the role played by them in brain ischemia reperfusionConsiderable studies on molecular mechanism of brain ischemia reperfusion had been conducted in recent years, including the changes of calcium homeostasis, the gengeration of free radicals and the disorder of mitochondria function, activation of protein kinase, and the expression of gene inflammation and so on. Among them, the disorder of mitochondria function plays an important role in brain ischemia reperfusion Injury. Aiming at the change of cytoplasm, mitochondria calcium homeostasis and disorder of mitochondria function, we discuss the role played by them in brain ischemia reperfusion injury

关 键 词：缺血性脑损伤 CA^2+超载 线粒体 神经保护治疗 再灌注时间 神经元死亡 溶栓治疗 脑损伤程度 

分 类 号：R651[医药卫生—外科学]