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作 者:王天懿[1] 孟庆颖[1] 朱玉群[1] 杨昭徐[1]
机构地区:[1]首都医科大学附属北京天坛医院消化内科,北京100050
出 处:《湖南中医药大学学报》2010年第4期60-63,共4页Journal of Hunan University of Chinese Medicine
摘 要:目的探讨创伤性脑损伤(TBI)并发应激性溃疡(SU)与内毒素血症(ET)和脂质过氧化(LPO)的关系。方法改良Feeney自由落体撞击法建立TBI模型。32只雄性Wister大鼠随机分4组:正常对照组、TBI后6、12、24 h组。计数溃疡指数(UI),光镜及电镜下观察胃黏膜和肝脏超微结构,测定血清ALT和AST、胃黏膜超氧化物歧化酶(SOD)和丙二醛(MDA)、血浆脂多糖(LPS)。结果 TBI后UI显著增加;超微结构显示胃黏膜、肝细胞不同程度受损;血清ALT、AST显著升高;胃黏膜SOD下降,MDA增加,分别与对照组比较有差异有统计学意义;血浆LPS显著升高,与ALT、AST和MDA显著正相关,与SOD显著负相关。结论 TBI后出现SU和肝损伤,ET和LPO可能是重要致病因素。Objective To explore the correlation between stress ulcer(SU) and endotoximia(ET) and lipid peroxidation(LPO) after traumatic brain injury(TBI). Methods The animal model of TBI was duplicated by modified Feeney' s. 32 male Wistar rats were randomly divided into control group and TBI 6, 12, 24h groups. The ulcer indexes(UI) and contents ofALT, AST, MDA, SOD and lipopolysaccharidc (LPS) were detected. Pathological changes were observed through both light microscope and electron microscopic. Results The UI grew significantly, as well as the values of ALT, AST and LPS in each TBI subgroup. Significant positive correlation was found between the values of LPS and ALT, AST, MDA, while significant negative correlation between the value of LPS and SOD. The injuries in both liver and gastric mucosal epithelial cells had been observed through both light and electron microscope. Conclusion ET and LPO may be involved in the pathogenesis of stress ulcer and liver injury after TBI.
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