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本文通过在21只家兔以闭塞双侧颈动脉及椎动脉法复制急性脑缺血模型,观察不同时相缺血及缺血再灌注各时相的β—EP活性变化,并同步监测了动物脑匀浆β—EP的含量。结果表明;脑缺血后各时相的β—EP较对照组显著升高(P<0.05);脑缺血30分钟后再灌注各时相的β—EP较单纯脑缺血组各时相升高更为显著(<0.05);缺血及缺血再灌流组动物海马及丘脑组织匀浆中的β—EP含量较对照组明显升高(P<0.05)。实验结果提示β-EP可能参了脑缺血及缺血再灌注后脑损伤的病理生理过程。
In this study, 21 rabbits were involved in occlusion of bilateral cerebral carotid artery and vertebral artery to establish acute cerebral ischemia model. The changes of β-EP activity at different phases of ischemia and ischemia-reperfusion phases were observed. Brain homogenate β-EP content. The results showed that the β-EP in each phase after cerebral ischemia was significantly higher than that in control group (P <0.05). After 30 min of cerebral ischemia, (P <0.05). The content of β-EP in hippocampus and thalamus homogenate was significantly higher than that in control group (P <0.05). The experimental results suggest that β-EP may participate in the pathophysiological process of brain injury after cerebral ischemia and reperfusion.