内毒素对大鼠继发性脑损伤与脑超微结构影响及甲基强的松龙干预的探讨  

The experimental study on the effect of endotoxin in secondary brain injury and brain ultrastructure in rat and the investigate of methylprednisolone in intervention

作　　者：徐晓筑[1] 齐玉昌[1] 廖银华[1] 陈敏[1] 

机构地区：[1]解放军44医院,贵阳550009

出　　处：《贵州医药》2002年第7期583-585,共3页Guizhou Medical Journal

基　　金：贵州省科学基金资助项目

摘　　要：目的观察内毒素对严重脑外伤后继发性脑损伤的影响 ,进一步探讨继发性脑损伤发生发展的机制及预防方法。方法建立大鼠脑挫裂伤模型 ,经腹腔注射内毒素 (致伤组 )及同时静脉给予甲基强的松龙 (干预组 )模拟脑外伤后经胃肠道移位途径 ,提高内毒素血症水平 ,观察伤后不同时相伤侧脑组织水份、钠、钾含量、伊文斯蓝染及病理、超微结构改变与对照组的比较。结果致伤组及干预组伤后 6h脑组织含水量及钠含量即明显高于对照组 (P <0 0 5 ) ;水肿高峰提前 ,较对照组有显著性差异 (P <0 0 1,P <0 0 5 ) ,致伤组较干预组水肿程度更重 (P <0 0 5 ) ;伤后 48h致伤组蓝染较干预组及对照组染色深、范围更宽 ;伤后 2 4h的病理、超微结构致伤组较对照组损伤明显加重 ,干预组介于二者之间。结论内毒素可显著加重脑外伤后继发性脑损伤的发生发展 ,早期使用甲基强的松龙可一定程度减轻其损伤作用。其机制可能 :(1)内毒素可直接损害血脑屏障 ,产生血管源性水肿 ;(2 )内毒素的细胞毒性及诱导炎性细胞因子增加可产生直接细胞损伤 ;(3)甲基强的松龙可抑制炎性细胞因子产生 ,从而预防二次打击的损伤作用。Objective To observe the effect of endotoxin in secondary brain injury after severe cerebral trauma, and to investigate the mechanism of the occurrence and development of secondary brain injury and preventing. Methods Cerebral contusion model of rat was established. Simulating the displacement way via gastrointestinal tract, endotoxin was injected into the abdomen of rat (injured group) and methylprednisolone was infected via vein synchronously (intervene group), to enhance the level of endotoxemia. The contents of water, sodium, kalium, the changes of pathology and ultrastructure were observed in the injured brain tissue during different time. Results Six hours after the trauma, compared with normal control, the contents of water and sodium in brain tissue were higher in injured group and intervene group (P<0.01, 0.05); the edema fastigium was brought forward obviously (P<0.05), and the edema degree of injured group was more seriously than in intervene group (P<0.05). 48 hours after the trauma, deeper and greater areas of blue dyeing were observed in injured group than in control and intervene group. Conclusions Early use of methylprednisolone may decrease the injury to some extent. The possible mechanisms are: 1. Endotoxin may cause the damage of blood brain barrier directly, and thus results in angio-edema. 2.The cytotoxicity of endotoxin and its inducing the increase of inflammatory cytoknes can give birth to direct cell injury. 3. Methylprednisolone can inhibit the production of inflammatary cytokines, thus prevent cells from secondary injury.

关 键 词：内毒素 继发性脑损伤 超微结构 甲基强的松龙 

分 类 号：R651.15[医药卫生—外科学]