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目的:探讨二次脑创伤后大鼠皮层脑血流(CoCBF)与前列腺素变化及双阿斯匹林联偶血红蛋白液(DCLHb)的作用。方法:在一种新的大鼠加速性弥漫性脑损伤模型基础上,采用抽血及颈动脉结扎造成低血压及脑缺血、缺氧,观察大鼠CoCBF与血栓素A2(TXA2)、前列环素(PGI2)含量变化以及DCLHb治疗作用。32只SD大鼠随机分为假手术对照、单纯脑损伤、脑损伤并二次脑创伤及治疗四组。所有动物均气管内插管并实施同步生理监护。结果:伤后4小时,与假手术组对比,合并二次脑创伤组CoCBF显著降低,TXA2含量增高(P<0.05);DCLHb治疗组无CoCBF降低,但TXA2及PGI2含量均有增高。结论:合并二次脑创伤组有CoCBF降低及TXA2含量增高,提示在其病理过程中存在脑血管痉挛及微血栓形成,导致脑缺血、缺氧。DCLHb则可能通过增加PGI2合成发挥脑保护作用。
Objective: To investigate the changes of cortical cerebral blood flow (CoCBF) and prostaglandin in rats after secondary brain injury and the effect of dual aspirin conjugated hemoglobin (DCLHb). Methods: Based on a new rat model of accelerated diffuse brain injury, hypotension and cerebral ischemia and hypoxia were induced by blood drawing and carotid artery ligation. CoCBF, TXA2, (PGI2) content changes and DCLHb treatment. Thirty-two Sprague-Dawley rats were randomly divided into four groups: sham operation control, simple brain injury, brain injury and secondary brain injury. All animals received endotracheal intubation and synchronized physiologic monitoring. Results: Compared with the sham-operation group, CoCBF and TXA2 increased significantly (P <0.05) at 4th hour after injury in rats. No decrease of CoCBF, but higher levels of TXA2 and PGI2 were found in DCLHb-treated group. Conclusion: CoCBF decreased and TXA2 level increased in the group of combined traumatic brain injury, suggesting cerebral vasospasm and microthrombus formation in the pathological process, leading to cerebral ischemia and hypoxia. DCLHb may play a role in brain protection by increasing PGI2 synthesis.