Hypotension is an infrequent but grave complication of acute pancreatitis and occurs in the earlier stages of severe necrosis. The question as to whether the hypotension is the systemic manifestation resulting from the entry of the pancreatic enzymes into the circulation, or whether the hypotension is the result of the local inflammatory exudate in and around the pancreas, has never been adequately determined. Clinical and experimental evidence has suggested that hypocalcemia,1 oligemia,2 and circulating serum trypsin3-14 might be responsible for the vascular collapse; but the correction of these factors sometimes fails to restore a normal blood pressure. Much of the literature has dealt with speculation as to whether circulating trypsin is a toxic factor in acute pancreatitis, which results in liberation of vasoactive substances through the plasma kallikreinogen-kininogen system. Others have suggested that kallikrein or possibly bradykinin or both might be released by the damaged pancreas into