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Intestinal Mucosal Hyperpermeability in Critical Illness

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Gut Dysfunction in Critical Illness

Part of the book series: Update in Intensive Care and Emergency Medicine ((UICM,volume 26))

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Abstract

The gut serves not only as a physiologic portal for the entry of water and nutrients into the body, but also as a barrier limiting the systemic absorption of intraluminal microbes and/or microbial products. The intestinal epithelium per se represents a critical barrier against systemic absorption of intralumenal microbes and microbial products. The ability of the intestinal epithelium to selectively permit the absorption of nutrients, electrolytes, and water, but restrict the passage from the lumen of larger, potentially toxic hydrophilic compounds is thought to be mediated by the tight junctions (“zonula occludens”) surrounding each cell in the epithelial sheet [1]. Under normal circumstances, tight junctions exclude passive movement of hydrophilic noncharged compounds with a molecular radius > 11.5 Å [1]. Substances that are therefore prevented from paracellular transepithelial movement include the amphipathic compound, lipopolysaccharide (LPS) [2], as well as a variety of other bacteria-derived proinflammatory hydrophilic compounds, such as formyl-methionyl-leucyl-phenylalanine (FMLP)

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© 1996 Springer-Verlag Berlin Heidelberg

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Fink, M.P. (1996). Intestinal Mucosal Hyperpermeability in Critical Illness. In: Rombeau, J.L., Takala, J. (eds) Gut Dysfunction in Critical Illness. Update in Intensive Care and Emergency Medicine, vol 26. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-80224-9_2

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  • DOI: https://doi.org/10.1007/978-3-642-80224-9_2

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