【摘要】 目的探讨早期联用美罗培南(MEP)和大剂量重组人生长激素(rhGH)对严重烫伤免疫抑制大鼠肠源性感染的影响。方法Wistar大鼠54只随机分为对照组、烧伤组和治疗组(C1组、C2组、C3组),后两大组制成25%总体表面积(TBSA)Ⅲ°烫伤免疫抑制模型,伤后2h给予rhGH1.33IU/kg、MEP20mg/kg,伤后8、24h检测门静脉血清内毒素(LPS)、腔静脉血清肿瘤坏死因子-α(TNF-α)含量,肝功能变化和肠道细菌移位率。结果C3(MEP+rhGH治疗)组LPS和TNF-α含量均显著低于其他组(P<0.01),与对照组差异无统计学意义(P>0.05),C3组未发现肠道细菌移位且肝功能检测指标显著低于其他组(P<0.01),与对照组差异无统计学意义(P>0.05)。结论早期联用MEP和rhGH治疗严重烫伤免疫抑制大鼠能显著减轻或防止肠道细菌/内毒素移位,减少炎症介质释放,保护脏器功能。更多还原

【Abstract】 Objective To investigate the effect of early use of meropenem(MEP) and large dose of recombinant human growth hormone(rhGH) on the enterogenic infection in severely scalded and immunosuppressive rats. Methods 54 adult male rats were randomly divided into control(A), scalded(B), and treated (C1=rhGH,C2=MEP,C3=MEP+rhGH) groups. Rats in the latter two groups were made into 25% TBSA Ⅲdegree scalded injury and immunosuppressive model. At 2 post burn hours(PBHs),hypodermic injection of rhGH with 1.33IU/kg or intramuscular injection of MEP with 20mg/kg was done on the rats in group C , while the rats in other groups were given normal saline(NS). Then detected these items at 8 and 24 PBHs: the level of lipopolysaccharide /endotoxin (LPS) in portal vein and the tumor necrosis factor alpha(TNF-a) in caval venous serum ,the hepatic function, and the rate of the intestinal bacteria translocation in the mesenteric lymph node (MLN),liver and kidneys. Results The levels of LPS and TNF-a in the rats of C3 group were markedly lower than that in other groups(P<0.01),but had not statistically significant difference compared with the A group(P>0.05).we had not found the bacterial translocation from intestine in the C3 group .The indices of hepatic function in the C3 group were significantly lower than those of other groups(P<0.01),but had not statistically significant difference compared with those of the A group(P>0.05).Conclusion Early use of MEP and large dose of rhGH to treat severely scalded and immunosuppressive rats, could remarkably prevent the intestinal bacteria/endotoxin translocation and decrease the release of mediators of inflammation, therefore protecting the hepatic function.更多还原