Experimental therapeutic strategies

A wide range of therapies have been shown to improve splanchnic blood flow in animal models of ischemia-reperfusion. These strategies have centered on inhibiting or inactivating polymorphonuclear adhesion and activation, as well as inhibiting the downstream consequences of such polymorphonuclear activation. Xanthine oxidase inactivation, phospholipase A2 inhibition, platelet activating factor antagonists, and P-selectin inhibition all inhibit polymorphonuclear sequestration in the splanchnic circulation after ischemia-reperfusion. Antibodies to IL-6 and IL-8 may also abrogate polymorphonuclear activation. The role of modulation of NO is unclear and may depend on ambient oxygen concentrations. While NO may protect the liver from lipopolysaccharide-induced injury, by acting as a vasodilator and partially reversing the effects of cytokines such as tumor necrosis factor-a, during ischemia-reperfusion No production may contribute to hepatic injury by combining with oxygen free radicals forming peroxynitrite. The therapeutic use of such strategies will require careful clinical trials.

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Sleep Apnea

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