Present concepts related to the pathogenesis of pancreatitis have implicated enzymes as an important factor in the initiation of the disease. As a consequence of ductal obstruction and hypertension, enzymes are thought to pass retrograde through minute clefts between the cells of the acinar unit to enter the interstitium of the gland.1-4Numerous studies have shown that the proteolytic enzyme, trypsin, infused into the pancreatic ducts, is capable of inciting an inflammatory response. Earlier findings suggest that trypsin affects the local pancreatic microcirculation by causing vasodilation, stasis, and increased capillary permeability.5When low concentrations of active trypsin were infused, pancreatic edema of variable intensity was produced, while higher concentrations resulted in a hemorrhagic interlobular extravasate. The mechanism by which trypsin causes these changes in local pancreatic circulation, and thereby initiates an inflammatory reaction, has been the topic of extensive investigation over the past few years. This protease has