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大鼠肠道屏障功能衰竭病因中的细菌过度生长与肠道萎缩

Bacterial overgrowth and intestinal atrophy in the etiology of gut barrier failure in the rat.

作者信息

Barber A E, Jones W G, Minei J P, Fahey T J, Lowry S F, Shires G T

机构信息

Laboratories of The Department of Surgery, Cornell University Medical College, New York, New York.

出版信息

Am J Surg. 1991 Feb;161(2):300-4. doi: 10.1016/0002-9610(91)91148-c.

DOI:10.1016/0002-9610(91)91148-c
PMID:1990885
Abstract

Bacterial translocation occurs in animal models of shock, trauma, sepsis, and parenteral or elemental enteral alimentation. Bowel atrophy and cecal bacterial overgrowth have both been implicated in the pathophysiology of bacterial translocation in many of these models. To further define the etiology of bacterial translocation resulting from dietary manipulations, rats were fed a elemental/defined-formula diet (DFD) for 2 weeks ad libitum and then randomized to either intestinal decontamination with a nonabsorbable antibiotic (neomycin) or no antibiotic treatment. Neomycin treatment significantly (p less than 0.01) reduced the incidence of bacterial translocation after DFD, in association with a significant reduction in the number of cecal gram-negative bacteria. Neither loss of bowel mass after DFD nor bowel composition was affected by oral neomycin. Bacterial translocation after DFD would thus appear to be the result of cecal bacterial overgrowth rather than a loss of a physical intestinal barrier due to atrophy.

摘要

细菌易位发生在休克、创伤、脓毒症以及胃肠外营养或要素肠内营养的动物模型中。在许多此类模型中,肠萎缩和盲肠细菌过度生长均与细菌易位的病理生理学有关。为了进一步明确饮食干预导致细菌易位的病因,给大鼠随意喂食要素/配方饮食(DFD)2周,然后将其随机分为两组,一组用不可吸收抗生素(新霉素)进行肠道去污处理,另一组不进行抗生素治疗。新霉素治疗显著(p<0.01)降低了DFD后细菌易位的发生率,同时盲肠革兰氏阴性菌数量显著减少。口服新霉素对DFD后肠质量的减少和肠组成均无影响。因此,DFD后的细菌易位似乎是盲肠细菌过度生长的结果,而非由于萎缩导致肠道物理屏障丧失所致。

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