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作 者:林洁[1] 李建英[2] 韦立新[3] 黄月红[4] 陈治新[4]
机构地区:[1]福建医科大学协和临床医学院,福州350001 [2]福建医科大学附属协和医院消化内科 [3]福建医科大学附属协和医院检验科 [4]福建医科大学附属协和医院消化内科研究所
出 处:《中华急诊医学杂志》2011年第5期502-506,共5页Chinese Journal of Emergency Medicine
摘 要:目的探讨前列腺素E1脂微球制剂(Lipo-PGEl)预处理对失血性休克复苏后大鼠肝损伤的保护作用及机制。方法32只健康雄性sD大鼠随机(随机数字法)分为4组(n=8),A:假手术组:B:休克组,休克90min后处死;C:失血性休克复苏组,大鼠麻醉后,经股动脉穿刺置管放血,使平均动脉压(MAP)降至(35±5)mmHg,维持90min,回输自体血液复苏,维持MAP80—100mmHg,制作失血性休克复苏模型;D:失血性休克复苏+Lipo—PGE1预处理组,Lipo—PGEI按10μg/kg溶于0.5mL生理盐水从股静脉注射,1h后制作失血性休克复苏模型。C组和D组于复苏后6h取血测肝功及NO、ET-1,HE染色观察肝组织病理变化,免疫组化检测肝组织iNOS和ET-1的表达。数据采用单因素方差分析,以P〈0.05为差异具有统计学意义。结果失血性休克复苏组肝脏发生严重缺血一再灌注损伤,ALT,AST,LDH及NO,ET-1较休克组均有不同程度升高(P〈0.05),肝组织iNOS和ET-1的表达显著高于休克组[(0.225±0.080)VS.(0.082±0.021),(0.292±O.047)VS.(0.082±0.035),P〈0.05];预先给药组肝脏病理损伤较模型组轻,ALT,AST,LDH及NO,ET-1较模型组均有不同程度降低(P〈0.05),肝组织iNOS和ET—1的表达明显低于模型组[(0.116±0.034)VS.(0.225±0.080),(0.198±0.041)VS.(0.292±0.047),P〈0.05]。结论Lipo—PGE1预处理可以减轻失血性休克复苏后大鼠肝损伤,其机制可能与抑制肝组织iNOS和ET-1的表达,调节NO/ET-1的平衡有关。Objective To observe the effects and mechanism of pretreatment in rats with prostaglandin El on liver after hemorrhagic shock and resuscitation(HSR). Method In total, 32 male SD rats were randomly ( random number) divided into four groups ( u = 8 ) : group A ( sham group) , group B ( shock group) , group C (HSR group) and group D (Lipo-PGE1 + HSR). In group B, rats were sacrificed 90 rain after shock, and in group C, rats were anesthetized and then subjected to hemorrhagic shock followed by re- suscitation. In group D, rats were pretreated with Lipo-PGE1 one hour before HSR. Liver function, NO and ET-1 were measured, and pathological changes of liver tissue in each group were observed, and the expres- sions of iNOS and ET-1 of liver tissue were measured by using immunohistochemistry 6 hours 'after HSR. Da- ta were analyzed by analysis of variance, and P 〈 0.05 was considered as significantly different in statitis- tics. Results The levels of liver iNOS and ET-I increased in HSR group compared with shock group [(0.225±0.080) vs. (0.082±0.021) and (0.292±0.047) vs. (0.082±0.035), P〈0.05 ]. Pre- treatment with Lipo-PGE1 markedly reduced the damage of Liver function, and lowered the levels of NO and ET-1, which were consistent with decrease in iNOS and ET-1 6 hours after HSR [ (0. 116±0. 034) vs. (0.225±0.080) and (0.198±0.041) vs. (0.292±0.047), P〈0.05]. Conclusions Pretreatmentwith Lipo-PGE1 could reduce liver injury after HSR. The mechanisms might be attributed to inhibiting iNOS and ET-1, regulating the balance of NO/ET-1.
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