Leukocyte activation in the splanchnic bed

In laboratory models, ischemia-reperfusion injury results in activation of membrane-bound phospholipase A 2. This enzyme catalyzes the production of the proinflammatory eicosanoids and platelet activating factor from membrane phospholipid. Both these substances can activate neutrophils and enhance their adhesion to endothelium. Platelet activating factor is also a potent mediator of vascular permeability. The gut mucosa contains substantial numbers of neutrophils, has a large surface area for the supply of membrane phospholipids, and has a particularly high concentration of xanthine oxidase which catalyzes the production of reactive oxygen species. This makes the gut a potent source of activated neutrophils. Gut ischemia followed by reperfusion increases vascular (and lung) permeability and causes pulmonary sequestration of neutrophils, and these effects can be abolished by inhibitors of phospholipase A 2 and neutrophil adhesion, and by leukocyte depletion (Biffl and Moore 1996). This process can occur in reverse; acid instillation into the lung produces gut mucosal leak, which can also be minimized by inhibitors of neutrophil adhesion to endothelium.

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