论文部分内容阅读
背景:颅脑损伤诱发的花生四烯酸代谢瀑布过程中产生的前列腺素类和氧自由基的增加是其重要的一方面,消炎痛能强烈抑制环氧化酶活性,减少前列腺素类合成,并可能减少氧自由基的增加,从而可能具有减轻脑损伤作用。目的:观察脑损伤后早期前列腺素的变化及消炎痛对其的干预作用,探讨其作用机制。设计:以实验动物为研究对象,随机对照实验研究。单位:一所大学医院的神经外科和一所大学医院的脑外科。材料:实验于2000-03/09在东南大学医学院神经外科实验室完成。将36只杂种猫,随机分为正常对照组,脑损伤组和消炎痛干预组3组,每组12只。干预:脑创伤按分级机械脑损伤实验动物模型制作,取中度脑损伤水平进行研究。伤后6h测定脑静脉血中前列腺环素(PGI2)和血栓素(TXA2)的最终分解产物6-酮-前列腺素F1a(6-keto-PGF1α)和血栓烷素B2(TXB2)、脑组织总超氧化物歧化酶(SOD)及脑含水量。主要观察指标:6-keto-PGF1α,TXB2,SOD含量和脑含水量测定。结果:猫脑损伤后早期脑静脉中6-keto-PGF1α和TXB2均明显增加犤由(0.057±0.010)g/L增至(0.264±0.126)g/L,由(0.060±0.012)g/L增至(0.134±0.048)g/L,6-keto-PGF1α增幅大于TXB2,TXB2/6-keto-PGF1α比值下降(由1.052±0.145降为0.545±0.184),脑含水量增加犤由(77.39±0.36)%增
BACKGROUND: The increase of prostaglandins and oxygen free radicals produced during traumatic brain injury-induced arachidonic acid metabolism falls is one of the important aspects. Indomethacin can strongly inhibit the activity of cyclooxygenase and reduce the synthesis of prostaglandins. And may reduce the increase of oxygen free radicals, which may have a role in reducing brain damage. Objective: To observe the changes of early prostaglandin after brain injury and the effect of indomethacin on it, and to explore its mechanism. Design: The experimental animals as the research object, randomized controlled experimental study. Unit: Neurosurgery at a university hospital and brain surgery at a university hospital. Materials: The experiment was performed at Neurosurgical Laboratory, School of Medicine, Southeast University from March to December in 2000. 36 hybrids were randomly divided into normal control group, brain injury group and indomethacin intervention group 3, 12 rats in each group. INTERVENTIONS: Brain trauma was made according to grading mechanical brain injury experimental animal model and moderate brain injury was studied. Six hours after injury, 6-Keto-PGF1α and TXB2, the final breakdown of prostacyclin (PGI2) and thromboxane (TXA2) in brain venous blood, Superoxide dismutase (SOD) and brain water content. MAIN OUTCOME MEASURES: Determination of 6-keto-PGF1α, TXB2, SOD and brain water content. Results: The levels of 6-keto-PGF1α and TXB2 were significantly increased in the early period of brain injury from (0.057 ± 0.010) g / L to (0.264 ± 0.126) g / L and from 0.060 ± 0.012 g / L (0.134 ± 0.048) g / L, the increase of 6-keto-PGF1α was more than that of TXB2, the ratio of TXB2 / 6-keto-PGF1α decreased from 1.052 ± 0.145 to 0.545 ± 0.184, 0.36)% increase