Acute pancreatitis after experimental pancreatic transplantation.

We describe our serendipitous finding of a transplantation model of hemorrhagic pancreatic necrosis. The slow evolution, from edematous interstitial pancreatitis to hemorrhagic necrosis over the course of 8 days made the model amenable to therapeutic manipulation. The possible pathogenesis is discussed with reference to the published literature. From comparisons between the histologic and biochemical features of isografts and allografts, we suggest that ischemia-reperfusion injury initiates pancreatitis through oxygen-free radicals, and that the transformation to hemorrhagic pancreatic necrosis in allografts reflects the involvement of chemotactic immune factors and extracellular secretions from activated proteases.