论文部分内容阅读
目的:探讨二次脑创伤(如低血压与高热)后大鼠脑血栓素A2(TXA2)与前列环素(PGI2)的代谢变化及意义。方法:在Marmarou弥漫性脑损伤模型基础上,采用抽血造成低血压,及高热形成二次脑创伤。32只SD大鼠随机分为假手术对照组、单纯脑损伤组、单纯二次脑创伤组及脑损伤合并二次脑创伤4组。所有动物均实施同步生理监护,伤后4小时检测脑内TXA2与PGI2的稳定代谢产物血栓素B2(TXB2)及6酮前列腺素F1α(6ketoPGF1α)含量。结果:伤后4小时,与假手术组比较,脑损伤组TXB2及6ketoPGF1α含量无明显变化;单纯二次脑创伤组仅6ketoPGF1α含量升高(P<0.05);合并二次脑创伤组TXB2及6ketoPGF1α含量均显著升高(P均<0.05),但TXB2/6ketoPGF1α比值下降。结论:原发脑损伤后,合并低血压与高热可使TXA2大量生成,通过引起脑血管痉挛及微血栓形成,增加脑微循环阻力,导致脑缺血、缺氧而加重原发性脑损伤。
Objective: To investigate the changes and significance of cerebral thromboxane A2 (TXA2) and prostacyclin (PGI2) after traumatic brain injury (such as hypotension and hyperthermia) in rats. Methods: Based on the Marmarou diffuse brain injury model, hypotension was induced by blood drawing, and secondary brain injury was formed by hyperthermia. Thirty-two Sprague-Dawley rats were randomly divided into 4 groups: sham operation control group, simple brain injury group, simple secondary brain injury group and brain injury combined with secondary brain injury. All animals underwent synchronous physiological monitoring. The stable metabolites of TXB2 and 6ketoPGF1α in TXA2 and PGI2 in brain were detected 4 hours after injury. Results: Compared with the sham-operated group, the levels of TXB2 and 6ketoPGF1α in the brain injury group were not significantly changed at 4 hours after injury. Only the contents of 6ketoPGF1α in the secondary brain injury group were significantly increased (P <0.05) And 6ketoPGF1α were significantly increased (all P <0.05), but the ratio of TXB2 / 6ketoPGF1α decreased. CONCLUSION: After primary brain injury, combined with hypotension and hyperthermia, TXA2 can be produced in large quantities. It can cause cerebral vasospasm and microthrombus formation, increase cerebral microcirculation resistance, lead to cerebral ischemia and hypoxia, and aggravate primary brain injury.