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目的:探讨远隔缺血后适应对局灶性脑缺血再灌注损伤后大脑梗塞面积及血脑屏障(blood brainbarrier,BBB)通透性功能障碍的保护性作用及其程度。方法:制备大鼠缺血再灌注损伤模型,建立远隔缺血后适应。应用TTC法评估脑梗死面积,采用干湿重法计算脑含水量评估脑水肿、应用伊文思蓝(Evans Blue,EB)观察再灌注后BBB通透性变化。结果:大鼠BBB通透性缺血后适应24 h组与缺血再灌24 h组相比明显减轻(P<0.05),缺血后适应48 h组与缺血再灌注48 h组相比明显减轻(P<0.05);TTC梗塞面积缺血后适应24 h组与缺血再灌注24 h组相比明显减轻(P<0.0001),缺血后适应48 h组与缺血再灌注48 h组比明显减轻(P<0.0001);缺血后适应组比缺血再灌注组脑含水量明显减少(P<0.01)。结论:缺血后适应能够保护缺血再灌注后血脑屏障的破坏,减轻梗塞面积和脑水肿。
Objective: To investigate the protective effects and the extent of post-ischemic postconditioning on cerebral infarction area and permeability dysfunction in the blood brain barrier (BBB) after focal cerebral ischemia-reperfusion injury. Methods: The rat model of ischemia-reperfusion injury was established, and the post-ischemic adaptation was established. The area of cerebral infarction was evaluated by TTC method. Brain edema was calculated by using wet and dry method to calculate brain water content. The permeability of BBB after reperfusion was observed by Evans Blue (EB). Results: The BBB permeability of 24 h group was significantly reduced compared with that of 24 h group (P <0.05), and 48 h after ischemia and 48 h after ischemia reperfusion (P <0.05). Compared with the 24 h group, the TTC infarct size of ischemic postconditioning group was significantly reduced (P <0.0001), the ischemic postconditioning 48 h group and the ischemia reperfusion 48 h group (P <0.0001). The content of water in the ischemic postconditioning group was significantly lower than that of the ischemia / reperfusion group (P <0.01). Conclusion: Post-ischemic postconditioning can protect the blood-brain barrier from ischemia-reperfusion injury and reduce the infarct size and cerebral edema.