“…Blood from patients with pancreatitis and from animals with experimental pancreatitis has been found to contain similar vasoactive material (Hollenberg, Kobold, Pruett, and Thal, 1962;Thal, Kobold, and Hollenberg, 1963). These substances are thought to be responsible for the production of hypotension, dehydration, and shock in severe pancreatitis, and a large number of papers has been published on the use of proteolytic enzyme inhibitors in experimental and human pancreatitis (Forell, 1962;McCutcheon and Race, 1963;McHardy, Craighead, Balart, Cradic, and LaGrange, 1963;Nardi, 1963;Moshal, Marks, Bank, and Ford, 1963;Schutt, Wakim, Bartholomew, Cain, and Baggenstoss, 1965) In relation to pathogenesis there is no evidence that kinins initiate pancreatitis although they are responsible for some of the clinical features; kinin production is secondary to the mechanism causing pancreatitis and is fired off by the presence of active trypsin. This process emphasizes further the basic importance of activation of proteolytic enzymes in the pathogenesis of pancreatitis.…”