Reperfusion injury in the equine intestine

摘要: At the cellular level, reperfusion of ischemic tissue results in rapid generation oxygen-derived free radicals, which overwhelm endogenous protective antioxidants and induce cell injury. Xanthine oxidase activation is key to post-ischemic mucosal injury small intestine, but lack significant xanthine dehydrogenase large colon suggests that an alternative source reactive oxygen species may prevail there. Endothelial cells regulate blood flow perfusion by altering balance endothelium-derived vasoconstrictors vasodilators, are considered be primary initiators Damage endothelium loss vasodilators (e.g. nitric oxide), causing increased sensitivity vasoconstrictive agents (certain eicosanoids endothelin-1). swelling also decreases tissue, a “no-reflow phenomenon.” stimulated radicals or platelets generate cytokines, attract activate neutrophils, thereby second phase The resulting characterized necrosis programmed death, apoptosis. Potential treatments horses include DMSO, manganese chloride, ascorbic acid, 21-aminosteroids, lidocaine, multimodal treatments, such as customized rinse solution Carolina Rinse. latter combination substances improve circulation, preserve endothelium, scavenge radicals. Evidence emerging about have potential facilitate repair, particularly specific COX-2 inhibitors glutamine.