反复性脑缺血大脑皮质LTC_4、cAMP和OFR的代谢变化  

Metabolic Changes of LTC_4, cAMP and OFR In the rat cerebral cortex following repeated global ischemia

作　　者：曹仁存[1] 郑彩梅[2] 欧阳尧[1] 

机构地区：[1]成都军区总医院神经内科,610083 [2]第三军医大学西南医院神经内科

出　　处：《脑与神经疾病杂志》2001年第2期68-70,共3页Journal of Brain and Nervous Diseases

基　　金："九五"军队医药卫生科研基金项目(96D040)

摘　　要：目的：研究反复脑缺血大脑皮质白三烯（ＬＴＣ４）、环腺苷酸（ｃＡＭＰ）和氧自由基（ＯＦＲ）的代谢变化与神经元损伤的关系。方法：对比观察大鼠反复性与单次性脑缺血大脑皮质ＬＴＣ４、ｃＡＭＰ、超氧化物歧化酶（ＳＯＤ）和丙二醛（ＭＤＡ）的含量变化及相应的病理改变。结果：反复缺血及再灌流早期ＬＴＣ１、ｃＡＭＰ的含量明显升高，ＳＯＤ活性显著降低，ＭＤＡ延迟性持续显著增高，皮质神经元损害显著重于单次缺血组。结论：ＬＴＣ４、ｃＡＭＰ和 ＯＦＲ均参与了反复缺血性脑损害的病理机制，可能与 Ｃａ＋＋介导的花生四烯酸（ＡＡ）瀑布效应有关。Objective: To study the relationship between the metabolic changes of cortical leukotrienesc4 (LTC4). cyclic AMP (cAMP) and oxygen free radicals(OFR )in the rat following repeated ischemic insults. Methods: The cortical LTC4. cAMP, superoxide dismutase (SOD), malondialdehyde(MDA) contents and pathological changes were observed following repeated cerebral ischemina in the rats or single ischemia. Results: The cortical LTC4 and cAMP contents in the repeated ischemic group were singnificantly higher, the SOD activity decreased singnificantly during ischemia and the early reperfusion, while the contents of MDA showed a delayed and long lasting increase, and the cortical neuronal injuries were found to be more sever in the group of repeated cerebral ischemia than those in the single ischemic insult group. Conclusion: The present results suggested that the LTC4, cAMP and OFR may participate in the pathogenesis of repeated cerebral ischemic damage, it may he due to the activation of arachidonic acid(AA) cascade by calcium-mdeiated reaction.

关 键 词：脑缺血 白三烯 环腺苷酸 自由基 大鼠 病理 

分 类 号：R743.302[医药卫生—神经病学与精神病学]