For many years the factors responsible for the systemic manifestations of acute pancreatitis have constituted a topic for speculation. The discovery in 1949 by Rocha e Silva of the vasoactive polypeptide bradykinin opened a new avenue of investigation.1 It brought to light a single substance capable of producing vasodilatation, increased capillary permeability, hypotension, polymorphonuclear leucocyte accumulation, and pain; all characteristic manifestations of acute haemorrhagic pancreatitis. In addition, the pancreas is known to contain large quantities of trypsinogen and kallikreinogen, both of which, in active form, are capable of releasing bradykinin from its inactive precursor bradykininogen. This precursor, in turn, is present as a pseudoglobulin in plasma, lymph, and interstitial fluid.
In a previous publication from this laboratory the hypothesis of kinin participation in the pathogenesis of acute pancreatitis was explored by Ryan et al.2 It was shown in dogs that bradykinin was released in shock-producing quantities when hemorrhagic