树鼩脑缺血后适应升高海马区rCBF及VEGF的变化  

Ischemic postconditioning increases the change of hippocampus rCBF and VEGF following cerebral Ischemic in tree shrews

作　　者：罗海芸[1] 李树清[1] 

机构地区：[1]昆明医学院病理生理教研室,云南昆明650031

出　　处：《基础医学与临床》2008年第7期676-680,共5页Basic and Clinical Medicine

基　　金：国家自然科学基金(3066005);教育部博士点专项科研基金(20050678008)

摘　　要：目的探讨缺血后适应(PC)缓解海马rCBF与血管内皮生长因子(VEGF)的变化及其机制。方法建立树鼩血栓性局部脑缺血模型,通过激光多普勒血流计测量海马CA1区rCBF含量;用免疫组化法测定海马VEGF的表达。结果树鼩脑缺血时海马rCBF逐渐降低,以24 h的改变最显著,脑缺血后海马CA1区VEGF阳性细胞数增多,12 h表达最强(P<0.01);缺血PC可显著影响缺血所致的改变:rCBF逐渐增加,72 h最显著(P<0.01),与此同时VEGF的表达除8 h外均比血栓性缺血组增强(P<0.01),12 h组最明显;电镜显示缺血24 h血栓性缺血组的海马线粒体应激及内质网池形成最明显,给予PC后得以缓解。结论缺血12 h内PC通过明显增强VEGF的表达可能与其改善rCBF有关,从而延长治疗的时间窗。Objective To find the effect and potential mechanism of ischemic postconditioning relief rCBF and VEGF expression during focal cerebral thrombosis. Methods The thrombotic focal cerebral ischemia was induced by photochemical reaction in tree shrews. The rCBF and VEGF expression in hippocampus CA1 area were detected, by laser-Doppler（LD） fowmeter and immunohistochemistry. Results rCBF reduces along with temporal lasting in cerebral thrombus, especially in 24 h; VEGF expression enhanced after cerebral ischemic, express of VEGF in 12 h is the most intensification （P 〈 0. 01 ）. Ischemic postconditioning may significant relieve the change of thrombotic focal cerebral ischemia：gradually increase hippocampus rCBF, especially in 72 h （ 10. 42 ± 3.75 PU, P 〈 0. 05 ） meanwhile the expression of VEGF was higher than that of ischemic except 8 h （P 〉0. 05）, mostly in 12 h （P 〈0. 01 ） ; Electron microscope revealed that mitochondrium stress and endoplasmic reticulum cisterna formation of hippoearnpus were the most manifest in 24 h, but when we apply postconditioning on it, the phenomenon can be relieived. Conclusion The protection mechanism of ischemic postconditioning may associate with the increase of rCBF in 12 h by intensification the express of VEGF, thus may prolong ＂time window＂ of therapeutic cerebral ischemia.

关 键 词：光化学 脑血栓 缺血后适应 血管内皮生长因子 局部脑血流 树鼦 

分 类 号：R743.32[医药卫生—神经病学与精神病学] R322.81[医药卫生—临床医学]