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作 者:许明伟[1] 许民辉[1] 赖西南 王丽丽[1] 张子焕[1] 崔红[1]
机构地区:[1]第三军医大学大坪医院野战外科研究所神经外科国家创伤烧伤与复合伤重点实验室,重庆400042
出 处:《创伤外科杂志》2010年第6期491-495,共5页Journal of Traumatic Surgery
基 金:全军"十一五"医学专项指令性课题(06Z034);国家科技支撑计划专项(2009BAI87B00)
摘 要:目的观察S-亚硝基谷胱甘肽(GSNO)在舱室内大鼠颅脑爆炸伤后继发性脑损伤中的作用,探讨其在舱室颅脑爆炸伤防治中的临床应用价值。方法 88只SD大鼠完全随机分为正常对照组(n=8)、单纯致伤组(n=40)和致伤+GSNO治疗组(n=40);采用二硝基重氮酚(DDNP)纸质点爆源在模拟装甲舱室爆炸,建立颅脑爆炸伤模型。伤后1、6、12、24、48小时取标本。测定脑组织中肿瘤坏子因子-α(TNF-α)、白介素-1β(IL-1β)浓度;丙二醛(MDA)浓度及超氧化物岐化酶(SOD)活性;观察脑组织病理学变化。结果致伤组伤后1小时脑组织TNFα-、IL-1β、MDA浓度均明显升高(P<0.01),伤后12小时升高达峰值(P<0.01),伤后48小时脑组织TNF-α、IL-1β浓度仍显著高于正常对照组(P<0.01)。致伤组伤后1小时脑组织SOD活性即显著降低(P<0.01),致伤后12小时降低至最低值(P<0.01),伤后48小时仍低于正常值。致伤组脑血管内皮细胞肿胀、脑水肿、神经元变性、坏死明显;给予GSNO治疗后各时间点脑组织TNF-α、IL-1β、MDA浓度均较致伤组明显降低,SOD活性明显增高(P<0.01或P<0.05)。治疗组脑水肿、神经元变性、坏死等表现均较单纯致伤组轻。结论舱室颅脑爆炸伤后可导致大鼠严重的继发性脑损伤;而早期给予GSNO可明显减轻脑组织炎性损伤和氧化损伤,减轻脑水肿及神经元变性、坏死,从而减轻继发性脑损伤。Objective To observe the effects of S-Nitrosoglutathione(GSNO) on secondary brain injury after explosive brain injury in enclosed space in rats,and explore the clinical value for GSNO in the fields of the therapy for explosive brain injury in enclosed space.Methods A total of 88 male Sprague-Dawley rats were divided randomly into normal control group(n=8),simple blast injury group(n=40),blast injury+GSNO group(n=40);and all rats were subjected to explosion with instantaneous electric detonator.Before and at 1,6,12,24 and 48 hours after injury,TNF-α and IL-1β concentration in brain were determined;MDA concentration and SOD activity in brain were determined.The pathological changes of brain were observed.Results The TNF-α,IL-1β and MDA concentration were significantly elevated at 1 hour after injury in simple blast injury group(P0.01),and elevated to the highest value at 12 hours after injury(P0.01).The value was still higher than normal control group at 48 hours after injury.The SOD activity was significantly reduced at 1 hour after injury in simple blast injury group(P0.01),and reduced to the lowest value at 12 hours after injury(P0.01).The value was still lower than normal control group at 48 hours after injury.After GSNO intervention,the TNF-α,IL-1β and MDA concentration were significantly reduced and SOD activity was significantly elevated than simple blast group(P0.01 or P0.05).Brain edema,neuronal degeneration and neuronal necrosis were attenuated in the blast injury + GSNO group.Conclusion Explosive brain injury in enclosed space could induce severe secondary brain injury,and administration of GSNO can relieve secondary brain injury after explosive brain injury.
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