Pancreatic duct mucosa following bile salt injury in cats

Autor: Marion Hänsler, Gerold Appelt, Thomas Arendt
Rok vydání: 1994
Předmět:
Zdroj: Digestive Diseases and Sciences. 39:1025-1033
ISSN: 1573-2568
0163-2116
DOI: 10.1007/bf02087554
Popis: We studied pancreatic duct mucosal morphology and barrier function to both activated and nonactivated pancreatic exocrine proteins following bile salt injury in cats. Prograde pancreatic duct perfusion with 15 mM glycodeoxycholate caused epithelial disruption with focal epithelial loss in the majority of animals. In these cats, flow of preanalyzed nonactivated rat pancreatic juice along the duct resulted in a selective loss of zymogens from the duct lumen as determined by two-dimensional isoelectric focusing-sodium dodecyl sulfate gel electrophoresis and reversed-phase high-performance liquid chromatography. Proteins lost had a low isoelectric point (≤5.7) and a molecular weight as large as 47,000 Da and included chymotrypsinogen 1, trypsinogens 1 and 2, and procarboxypeptidases B. Proteins with a high isoelectric point (>5.7), a high molecular weight (>47,000 Da), or both, were completely recovered from the duct lumen. Flow of activated rat pancreatic juice along a pancreatic duct with bile salt-induced epithelial disruptions caused additional morphologic alterations including an increase in epithelial destruction and occasional necrosis of the duct interstitial and vascular tissue. In some cats, in which the integrity of the ductal epithelium remained preserved following exposure to the bile salt, neither loss of rat pancreatic exocrine zymogens from the duct lumen nor degradation of the duct mucosa by activated rat pancreatic juice was observed. We conclude: (1) glycodeoxycholate-induced duct epithelial disruptions result in loss of pancreatic duct mucosal barrier function to pancreatic exocrine proteins; (2) pancreatic duct mucosal permselectivity to pancreatic exocrine zymogens following exposure to glycodeoxycholate is based on discrimination of molecular weight and charge, and the duct mucosa acts as a cationic charge selective macromolecular filter; and (3) glycodeoxycholate-induced duct epithelial disruptions render the MPD vulnerable to degradation by activated pancreatic juice. Thus, escape of pancreatic exocrine enzymes from the lumen of the MPD following bile salt injury may be due to both penetration across and/or degradation of the pancreatic duct mucosal barrier.
Databáze: OpenAIRE
Externí odkaz: