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.