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目的：观察醒脑静注射液(XNJI)对脑缺血再灌注家兔花生四烯酸代谢的影响，并探讨其脑保护机制。方法：将健康家兔20只以“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，造模后分为生理盐水组(n=10)和醒脑静组(n=10)，于缺血前和再灌注前，生理盐水组家兔静脉注射生理盐水1ml·kg~(-1)，醒脑静组静脉注射醒脑静注射液1ml·kg~(-1)。观察血浆、脑组织中血栓素B_2(TXB_2)、6-酮-前列腺素F_(1α)(6-Keto-PGF_(1α))含量与比值的变化，并观察脑超微结构变化。结果：醒脑静组与生理盐水组同时相相比血浆和脑组织TXB_2含量、TXB_2／6-Keto-PCF_(1α)比值明显降低(P＜0．05)，醒脑静组脑组织超微结构病理改变不明显。结论：XNJI通过抑制TXB_2合成、促进6-Keto-PGF_(1α)生成而下调两者比值，这可能是其减轻脑缺血再灌注损伤的又一作用机制。
Objective: To observe the effects of xingnaojing injection (XNJI) on the metabolism of arachidonic acid in rabbits with cerebral ischemia-reperfusion injury and to explore the mechanism of brain protection. Methods: Twenty rabbits were randomly divided into normal saline group (n = 10) and normal saline group (n = 10) by animal model of acute cerebral ischemia and ischemia reperfusion after “four tube occlusion” Xingnaojing group (n = 10). Before ischemia and before reperfusion, the rabbits in the saline group were injected with normal saline (1ml · kg ~ (-1)), Xingnaojing intravenously with Xinnaojing injection kg ~ (-1). The content and ratio of TXB2, 6-Keto-PGF_ (1α) in plasma and brain tissue were observed, and the ultrastructural changes of brain were observed. Results: The ratio of TXB_2 and TXB_2 / 6-Keto-PCF_ (1α) in plasma and brain tissue of Xingnaojing group was significantly lower than that of saline group (P <0.05) Structural and pathological changes are not obvious. CONCLUSION: XNJI can down-regulate the ratio of TXB2 synthesis and promote 6-Keto-PGF1α production, which may be another mechanism of its effect in reducing cerebral ischemia-reperfusion injury.