反复性脑缺血海马OFR的代谢变化  

Metabolic Changes of OFR in the Rat Hippocampus Following Repeated Global Ischemia

作　　者：曹仁存[1] 周厚永[1] 冉春梅[1] 

机构地区：[1]成都军区总医院神经内科,成都610083

出　　处：《西南军医》2007年第1期1-2,共2页Journal of Military Surgeon in Southwest China

摘　　要：目的研究反复性脑缺血海马氧自由基(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海马超氧化物歧化酶(SOD)和丙二醛(MDA)的含量变化及相应的海马神经元病理改变。结果反复缺血再灌早期SOD活性显著降低,MDA延迟性持续显著增高,海马神经元损害显著重于单次缺血组。结论OFR参与了反复性脑缺血海马神经元损伤和迟发性坏死(DND),并可能在该过程中起重要作用。Objective To study the relationship between the metabelic changes repeated cerebral isehemia. Methods The hippecrampal superoxide dismutase （ SOD）, malondialdehyde （ MDA ） contents and pathological changes were observed following repeated cerebral ischemia in the rats or single ischemia. Results The SOD activity decreased significantly during ischemia and the early reperfusion, while the contents of MDA showed a delayed and long-lasting increase, and the hippocampal neuronal injuries were found to be more severe in the group of repeated cerebral ischemia than those in the single ischemic insult group. Conclusion OFR is involved in the happecrampal neural damage and delayed neuronal death （DND） following repeated cerebral isehemia, and it may play a major role in the process.

关 键 词：脑缺血 反复性缺血 氧自由基(OFR) 海马 

分 类 号：R743[医药卫生—神经病学与精神病学]