2006
DOI: 10.1152/ajpgi.00377.2005
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Effects of pancreatic duct ligation on pancreatic response to bombesin

Abstract: . Effects of pancreatic duct ligation on pancreatic response to bombesin.

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Cited by 10 publications
(6 citation statements)
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References 16 publications
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“…Clinical and experimental observations suggest that pancreatic sensitization to potentially injurious stimuli has an important role in the pathogenesis of acute pancreatitis 8, 19, 20. The present study demonstrates that in both cellular and in vivo models of acute pancreatitis, an extracellular acid load sensitizes the acinar cell to secretagogue-induced zymogen activation and injury.…”
Section: Discussionsupporting
confidence: 52%
“…Clinical and experimental observations suggest that pancreatic sensitization to potentially injurious stimuli has an important role in the pathogenesis of acute pancreatitis 8, 19, 20. The present study demonstrates that in both cellular and in vivo models of acute pancreatitis, an extracellular acid load sensitizes the acinar cell to secretagogue-induced zymogen activation and injury.…”
Section: Discussionsupporting
confidence: 52%
“…Our survey of the literature revealed only one similar case, reported by Wright et al 11 Although the pathophysiology of the chronic obstructive pancreatitis in our patient involved a complex interaction of various factors, the retention of active pancreatic enzymes within the acinar cells and pancreatic ducts, and mechanical stress caused by high intraductal pressure might have played important roles in its development. 15,16 Five of the 12 patients presented with acute pancreatitis, and seven had recurrent pancreatitis. The histologic types of the neoplasms were adenoma in seven patients, carcinoma in adenoma in one, and carcinoma in four.…”
Section: Discussionmentioning
confidence: 99%
“…In a rodent model, acute pancreatic duct obstruction shift-ed acinar cell calcium signaling toward a pancreatitis phenotype (2). Acute duct obstruction followed by bombesin stimulation converted a physiologic pancreatic response to one associated with pancreatitis (3). Two additional observations were made in the PEP models developed by Rodger Liddle: (a) both increasing intraductal pressure and the composition of the fluid introduced affect disease development (4,5), and (b) the TRPV calcium channel could mediate this pancreatitis response (5).…”
Section: Calcium Signaling In the Pancreasmentioning
confidence: 99%