ISCHEMIA-REPERFUSION INJURY ON THE PANCREAS IN RATS - IDENTIFICATION OF ACINAR CELL APOPTOSIS

An ischemia-reperfusion injury on the pancreas is involved in the path ophysiology of acute pancreatitis or tissue injuries after pancreas tr ansplantation. On the other hand, recent studies have demonstrated tha t ischemia-reperfusion induces apoptosis in several organs such as kid ney, heart, and brain. In the present study, we sought to characterize a pattern of injury during ischemia-reperfusion on the pancreas and d etermined whether ischemia-reperfusion on the pancreas causes the apop totic process. Ischemia-reperfusion was induced by blocking the inferi or splenic artery and removing the clamp in pentobarbital-anesthetized rats. Rats were sacrificed at 0-72 hr following a 60-min ischemia. Ev ans blue extravasation showed 3.5-fold increase at 2 hr after reperfus ion, indicating a rapid increase of vascular permeability. Tissue myel operoxidase activity, an index of neutrophil accumulation, significant ly increased in a time-dependent manner until 48 hr after reperfusion. Histological analysis revealed the existences of interstitial cell in filtration and edema. DNA breaks of acinar cells were detected by gel electrophoresis and in situ nick end-labeling, and the numbers strikin gly increased at 48 hr after reperfusion. Furthermore, Bar protein, an effector of apoptotic cell death, was expressed in acinar cells. The results indicate that an ischemia-reperfusion injury on the pancreas i n rats resembles many features of acute pancreatitis. Apoptosis in aci nar cells may be one of the specific features of the ischemia-reperfus ion injury on the pancreas. (C) 1997 Academic Press.