Tubular complexes in cerulein- and oleic acid-induced pancreatitis in rats: glycoconjugate pattern, immunocytochemical, and ultrastructural findings

• Published in: Pancreas Vol. 2; no. 6; p. 669
• Main Authors: Willemer, S, Elsässer, H P, Kern, H F, Adler, G
• Format: Journal Article
• Language: English
• Published: United States 1987
• Subjects: Animals; Autoradiography; Ceruletide; Glycoconjugates - analysis; Immunohistochemistry; Lectins - metabolism; Male; Oleic Acid; Oleic Acids; Pancreas - immunology; Pancreas - metabolism; Pancreas - ultrastructure; Pancreatitis - chemically induced; Pancreatitis - metabolism; Pancreatitis - pathology; Rats; Rats, Inbred Strains
• ISSN: 0885-3177
• DOI: 10.1097/00006676-198711000-00008

Ductlike tubular complexes in cerulein-induced pancreatitis and oleic acid-induced pancreatic insufficiency were studied to analyze further their origin and development. Immunocytochemistry for pancreatic enzymes, lectin-binding studies, and ultrastructural investigations were combined with autoradiographic quantitation of labeling indices of ductlike cells in tubular complexes. In one group of rats, pancreatitis was induced by infusion of cerulein (10 micrograms kg-1 h-1). In a second group, pancreatic insufficiency was induced by intraductal injection of oleic acid (50 microliters). The investigations were carried out at distinct intervals following induction of pancreatic injury. In both groups of animals, after 3 days, a significant widening of acinar lumina was paralleled by a decreasing height of acinar cells, which showed pronounced retrogressive changes. At this time, acinar cells bound all of the lectins used and retained their immunoreactivity for amylase, trypsinogen, chymotrypsinogen, and lipase. At further intervals, acinar structures formed typical ductlike complexes, with a progressive loss of immunoreactivity for pancreatic enzymes and a reduced lectin-binding for L-fucose and N-acetylgalactosamine. Autoradiographic quantitation demonstrated no significant labeling of acinar cells undergoing tubular dedifferentiation. In both models, tubular complexes were removed by macrophages. It is concluded that lining cells in tubular complexes represent degenerating acinar cells that have no regenerative potency and have lost their secretory and membrane characteristics.