ISCHEMIA AND REPERFUSION IN PANCREAS

Ischemic diseases of heart and brain are the primary causes of mortali ty in industrialized nations. The ischemic injury with the consecutive reperfusion is responsible for the disturbance of microcirculation wi th ensuing tissue damage and organ dysfunction. Recent evidence sugges ts that oxygen-derived free radicals and activated polymorphonuclear l eukocytes produced in ischemic tissue are instrumental in the developm ent of ischemic cell injury. In pancreas, ischemia/reperfusion is prop osed as a potentially damaging factor accounting in part for the patho genesis of acute pancreatitis. Apart from ischemia/reperfusion injury, the kallikrein-kinin system mediates acute inflammation associated wi th enhanced capillary permeability and accumulation of polymorphonucle ar leukocytes, cardinal features of ischemia/reperfusion injury also i n acute pancreatitis. Therefore, it seems reasonable to use bradykinin -antagonists to influence postischemic reperfusion injury of the pancr eas. In the following, we describe the pathophysiology of ischemia/rep erfusion injury with special reference to the pancreatic microcirculat ion and morphological changes as observed in a model of complete and r eversible ischemia. Furthermore, we will discuss the effects of two br adykinin-antagonists (HOE 140 and CP-0597) on functional integrity of the pancreas after ischemia/reperfusion. (C) 1997 Wiley-Liss, Inc.