创伤性脑损伤后应激性肝损害及与肠源性内毒素血症的关系

Correlation of Hepatic Stress Injury with Gut-Origin Endotoximia after Traumatic Brain Injury

目的探讨创伤性脑损伤(TBI)后发生应激性肝脏损害(HSI)的机制及与肠黏膜屏障损伤和肠源性内毒素血症(GET)的关系。方法用改良Allen法建立TBI模型。40只健康雄性Wister大鼠随机分为5组:正常对照组、TBI后6、12、24、48小时时相组。测定肝血清酶、肝组织超氧化物歧化酶(SOD)、丙二醛(MDA)、血清肿瘤坏死因子-α(TNF-α)和血浆内毒素(脂多糖,LPS)水平,观察肝组织和肠黏膜超微结构的改变。结果TBI早期,各组血清丙氨酸氨基转移酶、天门冬氨酸氨基转移酶、TNF-α及LPS水平均升高,肝组织SOD减少、MDA增加,与对照组比较差异具有显著性(P<0.05,P<0.01);TBI各组LPS与肝血清酶、TNF-α及MDA呈显著正相关(P<0.05),与SOD呈显著负相关(P<0.05);TBI各组光镜和电镜下肝组织和肠黏膜上皮细胞均不同程度受损。结论TBI早期即出现肝脏和肠黏膜上皮的应激性损伤,HSI与GET和氧化应激等关系密切。

Objective mueosal barrier To explore the mechanism of hepatic stress injury （HSI） and the correlation with intestinal damage after traumatic brain injury （TBI）. Methods The animal model of TBI was established using a modified Allen＇s method. Forty healthy male Wistar rats were randomly divided into five groups： one control group （rats without operation） and four TBI group （6, 12, 24 and 48 hours after acute brain trauma）. The values of alanine aminotransferase （ ALT）, aspartate aminotransferase （ AST）, tumor necrosis factor-α（ TNF-α ）, malondialdehyde （ MDA ）, superoxide dismutase （ SOD ）, and lipopolysaccharide （ LPS ） were measured. The patlhological changes of liver tissue were observed under light and electron microscopy. Resuits The values of ALT, AST, MDA, TNF-α, and LPS increased and SOD decreased in each TBI subgroup at early period of TBI, which were significantly different from those in control group （P 〈0.05, P 〈0; 01 ）. The value of LPS was significantly correlated with the values of ALT, AST, TNF-α, and MDA （ P 〈 0.05 ） and negatively correlated with the values of SOD in each TBI subgroup （P 〈 0.05）. The injuries of liver tissue and intestinal mucosal epithelial ceils had been observed under light and electron microscope. Conclusions The stress injuries of liwer and intestinal mucosal epithelium occur at the early period of TBI. HSI is significantly correlated with gut-origin endotoximia and oxidative stress.