Abstract
Splanchnic ischemia-reperfusion, secondary to an interruption of blood supply or hypoperfusion, induces lesions of the intestinal mucosa and endothelial dysfunction. The consequences are at first an intestinal barrier failure with a defect for the entry of nutriments into the body. In parallel, splanchnic ischemia-reperfusion induces systemic inflammatory response. Gut reperfusion produces numerous mediators such as reactive oxygen metabolites, pro-inflammatory cytokines, nitric monoxide and activates numerous enzymes. The interaction between polymorphonuclear neutrophils and endothelial cells appear to play a key role in inducing damage to distant organ, particularly to the lungs. Briefly, splanchnic ischemia-reperfusion may be implicated in intestinal permeability, bacterial translocation and injury to distant organs. These effects are well observed in experimental models. In humans, the role of the gut remains always a controversial hypothesis. Nevertheless, the role of gut as a “motor of multiple organ failure” may be a tenable hypothesis, which warrants clinical research in this area.
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