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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.