Effects of short-term pancreatic duct obstruction in rats

Ohshio, Gakuji; Saluja, Ashok K.; Steer, Michael L.

doi:10.1016/0016-5085(91)90601-g

Cited by 101 publications

(60 citation statements)

References 11 publications

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“…Short-term (1-6 h) PDL in the rat has been found to cause pancreatic edema (11). Similar to our study, when secretin (another agent that does not cause pancreatitis) was superimposed on obstruction, edema increased.…”

Section: Discussionsupporting

confidence: 88%

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Effects of pancreatic duct ligation on pancreatic response to bombesin

Otani¹,

Matsukura²,

Takamoto³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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Section: Discussionsupporting

confidence: 88%

“…In this context, our study suggests that the acinar cell can respond with pathological zymogen activation even after PDL. This study confirms that when PDL is combined with an agent that does not cause pancreatitis, the combination causes pancreatic edema (11). In addition, it demonstrates that bombesin with PDL causes pancreatitis.…”

Section: Discussionsupporting

confidence: 77%

Effects of pancreatic duct ligation on pancreatic response to bombesin

Otani¹,

Matsukura²,

Takamoto³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…In 6-hr pancreatic duct ligation-induced pancreatitis, administration of T-0632 partially prevented both the increase in plasma amylase activity and the histological changes in the pancreas. Partially preventive effects of CCKA-receptor antagonists in this model have also been reported by others (10)(11)(12). On the other hand, CCKA-receptor antagonists have been reported to have no preventive effect on long-term pancreatic duct ligation induced pancreatitis (10).…”

Section: Discussionsupporting

confidence: 82%

Effect of T-0632, a CholecystokininA Receptor Antagonist, on Experimental Acute Pancreatitis.

Taniguchi¹,

Yomota²,

Kume³

et al. 1997

Jpn.J.Pharmacol

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“…These results confirm earlier observations reported by our group 4,16 using the opossum model and observations made by others who used different animal models. 33,34 Hepatic RES capacity was not significantly decreased in this mild form of pancreatitis. The results from groups A and B clearly indicate that neither RES dysfunction alone nor solitary pancreatic obstruction can cause necrotizing pancreatitis in this experimental setup.…”

Section: Discussionmentioning

confidence: 88%

Reticuloendothelial System Blockade Promotes Progression from Mild to Severe Acute Pancreatitis in the Opossum

Schleicher¹,

Baas²,

Elser³

et al. 2001

Annals of Surgery

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ObjectiveTo examine the relation between hepatic reticuloendothelial system (RES) dysfunction and the development of acute biliary pancreatitis. In an opossum model, the authors tested the hypothesis that RES blockade can turn the mild pancreatitis seen after pancreatic duct obstruction (PDO) into the severe form. Summary Background DataBiliary obstruction is considered the decisive event in gallstone pancreatitis. Suppression of the RES occurs during biliary obstruction. MethodsEighteen opossums were placed into three groups of six animals each: group A, RES blockade with -carrageenan; group B, PDO; and group C, PDO and RES blockade with carrageenan. The severity of pancreatitis was evaluated by enzyme serum levels and percentage of pancreatic tissue necrosis. RES capacity was measured by dynamic liver scintigraphy, and hepatic blood flow was documented using the hydrogen clearance technique. ResultsNo changes in hepatic blood flow occurred in groups A to C. RES capacity was suppressed in groups A and C; in group B, RES function remained unchanged. In group A, amylase and lipase levels remained normal, 3 Ϯ 1.9% of pancreatic tissue were necrotic. The animals in group B developed mild edematous pancreatitis with an increase in amylase and lipase levels and 15 Ϯ 10% of pancreatic necrosis. In group C, amylase and lipase increased significantly and histology revealed severe necrotizing pancreatitis, with 72 Ϯ 11% of necrotic areas. ConclusionsArtificial RES blockade can promote the progression from mild pancreatitis as observed after PDO to the severe necrotizing form of the disease. Thus, RES dysfunction resulting from biliary obstruction might be an important cofactor in the pathogenesis of bile-induced pancreatitis.Acute biliary pancreatitis is an inflammatory disease that varies in severity and outcome. Mild edematous pancreatitis usually results in morphologic and functional recovery, whereas severe necrotizing pancreatitis is often associated with multisystemic complications and a death rate of 10% to 50%. 1 The reason for this variety in manifestation is not known. The identification of factors determining the severity of acute pancreatitis is essential to improve the understanding of the pathophysiology of bile-induced pancreatitis and its complications.Obstruction of the terminal biliopancreatic ductal system is considered to be the triggering event in human gallstone pancreatitis. Opie, 2 in 1901, postulated that reflux of bile, caused by a gallstone impacted in a common terminal biliopancreatic duct, initiates the process of pancreatic inflammation. Today, most authors disagree with this socalled common channel theory, and not reflux of bile but simultaneous obstruction of the biliary and the pancreatic ducts and their pathophysiologic consequences are considered to be the determining factors in the development of severe pancreatitis.

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Effects of short-term pancreatic duct obstruction in rats

Cited by 101 publications

References 11 publications

Effects of pancreatic duct ligation on pancreatic response to bombesin

Effects of pancreatic duct ligation on pancreatic response to bombesin

Effect of T-0632, a CholecystokininA Receptor Antagonist, on Experimental Acute Pancreatitis.

Reticuloendothelial System Blockade Promotes Progression from Mild to Severe Acute Pancreatitis in the Opossum

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