INHIBITION OF POSTISCHEMIC REPERFUSION INJURY OF THE SMALL-INTESTINE BY DIAMINE OXIDASE

To elucidate the role of diamines in the pathogenesis of post-ischemic reperfusion-induced tissue injury, the effect of diamine oxidase was studied in the rat whose superior mesenteric artery was occluded for 15 min followed by 30 min reperfusion. Kinetic analysis using radiolabeled albumin revealed that the mucosal permeability of the reperfused small intestine increased significantly. Histological examination of the reperfused intestine revealed a marked degeneration of its mucosal layer. Intravenous administration of diamine oxidase inhibited the reperfusion-induced increase in mucosal permeability of the intestine almost completely and preserved the structure of the small intestine. H-1-antagonist chlorphenilamine and H-2-antagonist famotidine also inhibited the reperfusion injury of the small intestine. These and other results suggested that extracellular diamines might play critical roles in post-ischemic reperfusion-induced injury of the small intestine.