Determinants of gut permeability

The concept that the gut may cause systemic illness and remote organ injury dates from the end of the nineteenth century, and more recently phrases such as the gut being 'the motor of multiple organ failure' and 'the largest undrained abscess in the body' have established the theory in the medical imagination. Permeability of the gut mucosa has been studied using various molecular probes such as sugars or 51Cr-EDTA. Increased permeability has been demonstrated following many different physiological insults including ischemia-reperfusion injury, endotoxemia, systemic acidoses, glutamine deficiency, and certain cytokines such as g-interferon. One of several possible mechanisms for hyperpermeability is increased synthesis of nitric oxide by gut epithelium, neutrophils, or vascular endothelium. Nitric oxide may exert different effects on permeability depending on the nature of the stimulus, its timing, and the experimental model being used; these factors may explain why inhibition of nitric oxide synthase has been shown both to reduce and to increase gut permeability. However, the relevance of increased gut leakiness to translocation is uncertain, and it is possible that the phenomenon is merely a local expression of a generalized process.

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