作者: Emma Folch , Azucena Salas , Julián Panés , Emilio Gelpí , Joan Roselló-Catafau
DOI: 10.1097/00000658-199912000-00008
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摘要: Acute pancreatitis is an autodigestive process resulting in acute inflammation of the pancreas and systemic inflammation. In most severe forms pancreatitis, respiratory distress syndrome often occurs early stages disease can lead to death. 1 This lung injury characterized by increased pulmonary vascular permeability noncardiogenic edema. There evidence indicating that this mediated neutrophil infiltration. 2 The development inflammatory response involves sequential neutrophil–endothelial cell interactions described as rolling, activation, firm adhesion, migration. 3 These processes are controlled complex between surface receptors on neutrophils their corresponding endothelial ligands, designated selectins, integrins, or supergene immunoglobulins. Appropriate stimulation leukocytes cells results upregulation expression these molecules. particular, it has been reported 4 vitro xanthine oxidase-derived oxidants promote through intercellular adhesion molecule-1 (ICAM-1) P-selectin ligation. A growing body indicates causes a significant oxidant–antioxidant imbalance oxidative stress. 5 We have recently release oxidase from into bloodstream plays essential role pathogenesis complications including oxidant stress infiltration lung. 6 Conversion dehydrogenase (XDH) (XOD) acinar during action proteolytic enzymes activated consequence disruption. Accordingly, three main objectives study were investigate whether experimental rats upregulates molecules ICAM-1, unique feature generalized response; characterize ICAM-1 (as involved rolling adhesion) associated with means selective immunoneutralization; determine possible relation XOD-derived induction