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目的: 探讨醒脑静对脑缺血再灌注损伤保护作用及其可能机制。方法: 以“四管闭塞法”及再开放颈动脉建立家兔急性全脑缺血及缺血再灌注动物模型。随机分为对照组和用药组, 于缺血前和再灌注前对照组静脉注射生理盐水1ml/kg, 用药组静脉注射醒脑静1ml/kg。再灌注2h 后测定脑组织中血栓素B2(TXB2)、6 酮前列腺素F1α(6- Keto PGF1α)含量及其比值, 并观察脑超微结构变化。结果: 用药组脑组织TXB2 含量、TXB2/6 -Ke to PGF1α比值明显降低(P<0 .05), 脑组织超微结构病理改变明显减轻。结论: 醒脑静对脑缺血再灌注损伤具有保护作用, 其可能机制与调节花生四烯酸的代谢平衡有关。
Objective: To investigate the protective effect of Xingnaojing on cerebral ischemia-reperfusion injury and its possible mechanism. Methods: A rabbit model of acute global cerebral ischemia and ischemia / reperfusion was established by “four tube occlusion method” and reopened carotid artery. Randomly divided into control group and medication group, before ischemia and before reperfusion, the control group received intravenous injection of normal saline (1ml / kg) and the drug group received intravenous xingnaojing (1ml / kg). The contents of thromboxane B2 (TXB2) and 6-Keto PGF1α in brain tissue were measured 2h after reperfusion, and their ultrastructural changes were observed. Results: The content of TXB2 and the ratio of TXB2 / 6-KeE to PGF1α in the treated group were significantly decreased (P <0.05), and the pathological changes in the ultrastructure of the brain tissue were relieved. Conclusion: Xingnaojing has a protective effect on cerebral ischemia-reperfusion injury, and its possible mechanism is related to the regulation of arachidonic acid metabolism balance.