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脑内血栓素A₂(TXA₂)和前列环素(PGI₂)水平与继发损伤的弥漫性脑损伤相关。

Brain TXA(2)and PGI(2)levels related to diffuse brain injury with secondary insults.

作者信息

Zhou F, Xiang Z, Yu YS, Jun SS, Piper IR, Thomson D, Miller JD

机构信息

Department of Neurosurgery, Xijing Hospital, Xian, 710032, P.R. China

出版信息

J Clin Neurosci. 1999 Jul;6(4):306-308. doi: 10.1054/jocn.1997.0058.

Abstract

Secondary insults such as hypotension and hypoxia with head injury are associated with increased mortality and morbidity in comparison with head injury alone. In the present study the changes of brain thromboxane A(2)(TXA(2)) and prostacyclin (PGI(2)) levels in a Marmarou's rodent model of diffuse brain injury with hypotension and hypoxia were observed and the effect of diaspirin cross linked haemoglobin solution (DCLHb) were also investigated. Thirty-two male Sprague-Dawley (SD) rats were randomized into four groups: sham; head injury alone; head injury with secondary insults; and injury with insults followed by DCLHb administration. The results showed that there were no changes in TXB(2)and 6-keto-PFG(1a)(metabolites of TXA(2)and PGI(2)) levels in the injury alone group, while TXB(2)levels in the secondary insults group were elevated significantly; both TXB(2)and 6-keto-PGF(1a)levels in the injury with insults followed by DCLHb administration group were augmented significantly in comparison with the corresponding value of sham at 4 postimpact. The only increase in TXA(2)levels in the secondary insults rats suggests that an imbalance in TXA(2)-PGI(2)production contributes to the traumatic secondary processes, which include ischaemia and oedema. It is hypothesized that DCLHb may exert its protective properties through increasing PGI(2)production in injured brain by improving blood supply to injured blood vessels. Copyright 1999 Harcourt Publishers Ltd.

摘要

与单纯头部损伤相比,头部损伤合并低血压和低氧等继发性损伤会增加死亡率和发病率。在本研究中,观察了Marmarou啮齿动物弥漫性脑损伤合并低血压和低氧模型中脑血栓素A2(TXA2)和前列环素(PGI2)水平的变化,并研究了双阿司匹林交联血红蛋白溶液(DCLHb)的作用。32只雄性Sprague-Dawley(SD)大鼠被随机分为四组:假手术组;单纯头部损伤组;头部损伤合并继发性损伤组;损伤合并继发性损伤后给予DCLHb组。结果显示,单纯损伤组TXB2和6-酮-PGF1α(TXA2和PGI2的代谢产物)水平无变化,而继发性损伤组TXB2水平显著升高;与撞击后4小时假手术组相应值相比,损伤合并继发性损伤后给予DCLHb组TXB2和6-酮-PGF1α水平均显著升高。继发性损伤大鼠中仅TXA2水平升高表明TXA2-PGI2产生失衡导致包括缺血和水肿在内的创伤性继发过程。推测DCLHb可能通过改善损伤血管的血液供应,增加损伤脑内PGI2的产生而发挥其保护作用。版权所有1999年Harcourt出版有限公司。

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