Disruption of the intestinal barrier and bacterial translocation in an experimental model of intestinal obstruction.

Acta cientifica venezolana Pub Date : 2000-01-01
R Antequera, A Bretaña, A Cirac, A Brito, M A Romera, R Zapata
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Abstract

Clinical evidence and the use of experimental models in laboratory animals indicate that the intestine is a reservoir of microorganisms that can cause systemic infection in the human. The purpose of this work was to study the possible effect of intestinal obstruction (IO) on the mechanical and chemical barriers that bring protection against microorganisms crossing from the intestinal lumen towards the systemic tissues. We demonstrated that 24 hours after IO, histological and ultrastructural alterations do occur, seriously compromising the structure of the intestinal barrier in 100% of the studied animals. Likewise, it was observed that during the same period, microorganisms translocation from intestine to the peritoneal cavity and liver (100 and 80% respectively) occurred. The lungs were spared. Changes observed in the intestinal epithelium are related to a process similar to that produced by intestinal ischemia: mitochondrial destruction, with subsequent decrease of its capacity to supply energy and to preserve the equilibrium and structure of the intestinal epithelium. We propose that translocation of enteric bacteria may be the cause of the infection that brings about the death a significant group of animals at 48 hours (27%) and 72 hours (33%) post-IO.

肠梗阻实验模型中肠屏障的破坏和细菌移位。
临床证据和在实验动物中使用的实验模型表明,肠道是可引起人类全身性感染的微生物的储存库。这项工作的目的是研究肠梗阻(IO)对防止微生物从肠腔进入全身组织的机械和化学屏障的可能影响。我们证明,在肠内注射24小时后,组织学和超微结构确实发生改变,严重损害了100%被研究动物的肠屏障结构。同样,在同一时期,微生物也发生了从肠道到腹腔和肝脏的易位(分别为100%和80%)。肺部没有受到影响。在肠上皮中观察到的变化与肠缺血产生的过程类似:线粒体破坏,随后其供应能量和保持肠上皮平衡和结构的能力下降。我们认为肠道细菌的易位可能是导致大量动物在io后48小时(27%)和72小时(33%)死亡的感染原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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