CURRENT CONCEPTS emphasize the importance of pancreatic duct obstruction, combined with exocrine hypersecretion, as an important mechanism responsible for the initiation of pancreatic inflammatory disease.1Duct hypertension is associated with the release of pancreatic enzymes into the interstitial areas of the gland and is manifested clinically by pain, nausea, and vomiting. Recent studies have shown that proteolytic enzymes, introduced into the interstitial tissues, increase the permeability of local pancreatic blood vessels.2Fluid extravasted into the interlobular areas varied from a simple serous type of transudate to a grossly bloody fluid, depending upon the amount of enzyme injected. Earlier studies have confirmed that an incubated mixture of autologous whole blood and trypsin produced severe necrosis when injected into the pancreatic ducts of dogs.3Nemir and his associates were first to describe this phenomenon; they demonstrated the presence of an abnormal hemin pigment in enzyme-digested blood.4Our