二次脑创伤后大鼠皮层脑血流及前列腺素变化及血红蛋白液的作用

Cerebral blood flow and brain TXA2 and PGI2 levels in a rodent model of diffuse brain injury with secondary insults

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 significance of cortical cerebral blood flow (CoCBF) and brain TXA2 and PGI2 levels in a rodent model of diffuse brain injury with secondary insults. Methods:The changes of CoCBF and brain TXA2 and PGI2 (a pair of potent cerbral vasoconstrictor and vasodilator) levels in a rodent model of impact acceleration diffuse brain injury with hypotention made by blood withdrawing and hypoxia made by carotid artery occlusion were observed and the effect of Diaspirin cross linked hemoglobin sloution (DCLHb) also investigated, 32 male SD rats were randomized into 4 groups sham, head injury alone, head injury with secondary insults and injury with insults followed by DCLHb administration. All animals were intubated and physiologically monitored minute by minute. Results: Compared with that of sham group, there was a decreased mean CoCBF and elevated TXB2 level in head injury with secondary insults group. However, There was no change in mean CoCBF but TXB2 and 6ketoPGFla levels in injury with insults followed by DCLHb administration augmented significantly in comparison with the correspoining of sham at 4 hours postimpact. Conclusions:The increase in TXA2 level in head injury with secondary insults rats suggests that both thrombotic episodes and vasoconstriction may lead to focal increase in microcirculatory resistance which contributes to the decreased focal CoCBF. And it is hypothesized that DCLHb may exert its protective properties through increasing PGI2 production in injured brain by affecting cerebal blood flow and cerebral perfusion pressure.