Open AccessExperimental Gallstone Pancreatitis
Author(s) -
Patrick J. Broe,
John L. Cameron
Publication year - 1982
Publication title -
annals of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.153
H-Index - 309
eISSN - 1528-1140
pISSN - 0003-4932
DOI - 10.1097/00000658-198205000-00005
Subject(s) - hyperamylasemia , medicine , pancreatitis , extravasation , secretin , pancreatic duct , gastroenterology , endocrinology , amylase , pathogenesis , pancreas , albumin , pathology , enzyme , biochemistry , chemistry
Partial pancreatic duct obstruction due to gallstone migration has been suggested as an important step in the pathogenesis of gallstone, pancreatitis. Since gallstone migration often follows a meal, pancreatic secretory stimulation is also present. Utilizing the isolated perfused canine pancreas, an experimental model of gallstone pancreatitis was developed by partial obstruction of the main pancreatic duct and secretin stimulation (POSS). In control glands (n=6) perfused for a four-hour period, gross appearance remained normal, weight gain (8 g) was minimal, and mean amylase (875 Caraway units/dl) remained within normal limits. POSS glands (n=9) became markedly edematous during the perfusion period, with significant weight gain (47 g) and hyperamylasemia (7200 Caraway units/dl). Steroid-treated (n=6) and Trasylol-treated (n=6) POSS glands became edematous, and mean weight gain and hyperamylasemia were similar to those seen in untreated POSS glands. Glucagon-treated POSS glands (n=6) became edematous, but mean weight gain (24 g) was significantly decreased compared with that of untreated POSS glands. Mean amylase elevation was unchanged (8536 Caraway units/dl). POSS glands treated with albumin (n=6) remained normal in gross appearance, mean weight gain (12 g) was minimal and mean amylase (3120 Caraway units/dl) was significantly decreased compared to that of untreated POSS glands. The failure of Trasylol to ameliorate the injury response and the effectiveness of albumin were interpreted as evidence against enzyme extravasation and for capillary injury as the initial step in the pathogenesis of gallstone pancreatitis.