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Experimental Study of Interstitial Injection of Trypsin and Trypsinogen into the Pancreas
LUTHER M. KEITH, Jr., M.D.;
JAMES E. BARNES, M.D.;
FRED R. DENKEWALTER, M.D.
AMA Arch Surg. 1958;77(3):416-420.
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Many of the factors in the pathogenesis and experimental production of acute pancreatitis are conflicting and controversial. It is generally conceded that interstitially extravasated, active trypsin in the pancreas plays a dominant role.1,2 Evidence further indicates that if, in addition, ductal obstruction or ischemia supervenes, necrotic or hemorrhagic pancreatitis is likely to ensue.1-4 The pivotal issues seem to be (1) the mechanism by which trypsin or trypsinogen is extravasated, (2) whether trypsinogen itself can cause pancreatitis, and (3) the manner in which trypsinogen is activated.
The majority of investigators have utilized ductal perfusion of bile or pancreatic juice.1,3 Stein and co-workers have produced hemorrhagic pancreatitis by injection of trypsin into the dog's pancreaticoduodenal artery and ligation of the pancreatic ducts. Hosie and Ziffren5 have implicated collagenase, normally contained in pancreatic juice, as the initiator of pancreatitis. Since much of the experimental evidence indicating active trypsin as
. . . [Full Text PDF of this Article]
Author Affiliations
Columbus, Ohio
From the Department of Surgery and the Surgical Laboratories, Ohio State University College of Medicine and University Hospital. Aided in part by a grant from the Comly Fund.
Footnotes
Submitted for publication March 28, 1958.
Read at the 15th Annual Assembly of the Central Surgical Association, Columbus, Ohio, Feb. 21, 1958.
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