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March 1968

Failure of a Potent Trypsin Inhibitor to Modify Experimental Pancreatitis in Dogsp-Aminobenzamidine

Author Affiliations

Chapel Hill, NC
From the Department of Pathology, University of North Carolina School of Medicine, Chapel Hill, NC.

Arch Surg. 1968;96(3):450-457. doi:10.1001/archsurg.1968.01330210128026

NUMEROUS THEORIES have been advanced to explain the cause of pancreatitis, and many experimental models have been devised to simulate the proposed pathogenetic mechanisms. The concepts differ mainly in their interpretation of the initial events that lead to the disease, but nearly all of them postulate that there is intrapancursors and that the active enzymes are responsible for many of the local as well as systemic pathologic effects. Trypsin is thought to be formed first, possibly under the influence of cathepsins,1,2 and this is to result in the autocatalytic activation of more trypsinogen and also in the activation of chymotrypsins, procarboxypeptidases, and kallikreinogen. The circulatory changes which dominate the clinical picture are generally related to the release of bradykinin and kallidin,3-5 two vasoactive peptides which are split off kininogen by the proteolytic activity of trypsin and kallikreins. In addition, hypotensive amines, such as histamine, are possibly set free

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