Abstract
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 allograf ts reflects the involvement of chemotactic immune factors and extracellular secretions from activated proteases. © 1989.
| Original language | English |
|---|---|
| Pages (from-to) | 452-458 |
| Number of pages | 6 |
| Journal | American Journal of Surgery |
| Volume | 158 |
| Issue number | 5 |
| Publication status | Published - Nov 1989 |