Ligation-Induced Acute Pancreatitis Increases Pancreatic and Circulating Trypsinogen Activation Peptides

Merriam, Louis T.; Wilcockson, Daniel P.; Samuel, Isaac; Joehl, Raymond J.

doi:10.1006/jsre.1996.0068

Cited by 13 publications

(6 citation statements)

References 2 publications

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“…However, the view that the mechanical increase in intraductal pressure leads to the release of enzymes from the acinar cells into the parenchyma is finding credence by most authorities [5,17]. This study shows that intraductal infusion of contrast and increased pressure possibly has an aggravating effect on the pathogenesis of pancreatitis.…”

Section: Discussionmentioning

confidence: 71%

The effects of contrast agent and intraductal pressure changes on the development of pancreatitis in an ERCP model in rats

Haciahmetoglu

Ertekın

Dolay

et al. 2007

Langenbecks Arch Surg

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Section: Discussionmentioning

confidence: 71%

The effects of contrast agent and intraductal pressure changes on the development of pancreatitis in an ERCP model in rats

Haciahmetoglu

Ertekın

Dolay

et al. 2007

Langenbecks Arch Surg

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“…The results for water content from unstimulated and caerulein-hyperstimulated samples are consistent with those reported in the literature (unstimulated, 72-74% water content; caerulein hyperstimulated, 86 -89%). Although edema has been reported to occur after PDL in other studies, the study periods were all greater than the 3 h used in this study (9,10).…”

Section: Resultsmentioning

confidence: 93%

“…The observation that there is prominent accumulation of TAP within the acinar cell only when PDL was combined with bombesin is consistent with the hypothesis that PDL inhibits acinar cell secretion. Previous studies have suggested that acinar cell secretion from zymogen granules is inhibited by pancreatic duct obstruction (6,9). Because zymogens appear to be activated in and secreted from nonzymogen granule compartments (6,13), it was unclear whether they would exhibit the same inhibitory response to PDL.…”

Section: Discussionmentioning

confidence: 99%

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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“…All groups of rats were sacrificed and sampled 4.5 hours following the ligation or sham ligation of the pancreatic duct. This time point was selected based on data demonstrating that structural and functional pancreatic changes, as well as α-amylase levels, had not yet peaked thereby allowing us to correlate mucus and gut permeability changes with the onset of early acute pancreatitis (22,23). Using these three groups of rats, two sets of experiments were conducted.…”

Section: Methodsmentioning

confidence: 99%

The Intestinal Mucus Layer is a Critical Component of the Gut Barrier that is Damaged During Acute Pancreatitis

Fishman¹,

Levy²,

Alli³

et al. 2014

Shock

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Background Gut barrier failure has been implicated in the progression from single organ injury to multiple organ failure. The unstirred mucus layer is a major component of the physiological gut barrier, its role in acute pancreatitis(AP) is not clearly defined. Study Design Rats underwent biliopancreatic duct ligation-induced AP; two controls were used: biliopancreatic duct ligation with drainage and sham duct ligation. After 4.5 hours, serum and ascitic amylase activity was measured. Mucus was analyzed for reactive nitrogen intermediates(RNI)-mediated damage, reactive oxygen species(ROS)-induced damage, and total antioxidant capacity. Mucus coverage and villous injury was assessed histologically. Ileum permeability was measured by diffusion of a fluorescent dextran probe. Histology and morphology of the mucus layer were validated in a mouse AP model (intraductal taurocholate plus caerulein). Results Biliopancreatic duct ligation increased serum α-amylase, ascitic volume, and ascitic α-amylase. Intestinal permeability was increased, which was associated with loss of the unstirred mucus layer but not villous injury. These changes correlated with increased ROS-and-RNI-mediated mucus damage as well as decreased mucus total antioxidant capacity but were not present in the two control groups. Using a different model of AP in mice, the finding of mucus layer disruption was recapitulated at 6 hours after AP, but by 24 hours, rebound hypersecretion of inspissated mucus was seen. Conclusions These results support the hypothesis that damage to the unstirred mucus layer with evidence of oxidative stress occurs during AP-induced gut barrier failure.

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Ligation-Induced Acute Pancreatitis Increases Pancreatic and Circulating Trypsinogen Activation Peptides

Cited by 13 publications

References 2 publications

The effects of contrast agent and intraductal pressure changes on the development of pancreatitis in an ERCP model in rats

The effects of contrast agent and intraductal pressure changes on the development of pancreatitis in an ERCP model in rats

Effects of pancreatic duct ligation on pancreatic response to bombesin

The Intestinal Mucus Layer is a Critical Component of the Gut Barrier that is Damaged During Acute Pancreatitis

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