氧自由基损伤在烫伤大鼠延迟复苏后肠道细菌和内毒素移位中的作用

Dtlayed fluid resuscitation induced bacterialtranslocation after lethal therhtal injury:role of oxygenfree radical injury of intestinal mucosa

为了了解烧伤延迟复苏后肠粘膜氧自由基损伤情况及其对肠源性细菌、内毒素移位的影响，将６６只悉生大鼠分为以下四组：（１）对照组（ｎ＝６）。（２）立即复苏组（ｎ＝２４），４０％烫伤后立即按Ｐａｒｋｌａｎｄ公式复苏。（３）延迟复苏组（ｎ＝２４），伤后６小时开始复苏。（４）药物治疗组（ｎ＝１２），大鼠延迟复苏加上维生素Ｃ、Ｅ联合治疗。在伤后８、２４、４８和７２小时活杀动物（各时间点６只）进行下列指标检测：回肠粘膜超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨＰｘ）及丙二醛（ＭＤＡ）含量，回肠粘膜病理形态学观察、二胺氧化酶（ＤＡＯ）活性，血和肠系膜淋巴结、肝、脾、肾、肺细菌培养，血浆内毒素水平。结果显示，伤后ＳＯＤ、ＧＳＨＰｘ含量下降，ＭＤＡ升高，同时肠粘膜病理改变加重、ＤＡＯ活性下降，血和脏器细菌移位率、血浆内毒素水平增高。这些改变在延迟组更明显，使用维生素Ｃ、Ｅ治疗后减轻。表明，烧伤延迟复苏加重肠粘膜氧自由基的损伤，促进肠道细菌和内毒素移位。

The Present investigation was undertaken to ex-amine the effect of delayed fluid resuscitation (DFR).after lethal thennal injury on oxygen free radical(OFR) injury of intestinal mucosa and its relationshipto bacterial translocation. Four groups of gnotobioticrats with 5 strains of bacteria were studied: sham injury group (control) (n=6); early fluid resuscitation(EFR) group (n=24) receiving resuscitation(parkland) immediately after sculd (40% TBSA, thirddegree): DFR group (n = 24) receiving resuscitation 6hours after scald; treatment group (n = 12), rats withDFR receiving VitE and VitC treatment before resus-citation 12, 24, 48 and 72 hours after injury, animals(n=6, at each point) were sacrificed. Plasmaendotoxin level, mucosal SOD. GSHPx. MDA anddiamine oxidase (DAO) of ileum were determined, andcultures of the mesentenc lymph nodes (MLN), liver,spleen, heart, lung, kidney and blood were done. Thelevel of mucosal MDA and plasma endotoxin and theincidence of bactena translocation (IBT) to tissueswere significantly higher and mucosal SOD, GSHPx,DAO activity significantly lower in DFR group ascompared with that in EFR group at most of the timepoints. In DFR group, mucosal MDA content wasnegatively correlated with mucosal DAO activity,which correlated positively with plasma endotoxin ley-el and IBT. After treatment with VitE and VitC.mucosal MDA content was decreased, plasmaendotoxin level and IBT were significantly decreased,and mucosal DAO activity was significantly increased.Our data indicated that DFR in cases of burn shockcan result in OFR injury of intestinal mucosa, dis-rupting mucosal barrier and promoting translocationof intestinal bacteria and endotoxin.