title: Exocrine pancreatic function in obstructive jaundice rats: studies with isolated dispersed pancreatic acini.
abstract: This study was conducted to investigate pancreatic exocrine function and pancreatic growth in rats with obstructive jaundice (OJ). OJ was produced in adult male Sprague-Dawley rats by bile duct ligation; control rats underwent laparotomy only. Induction of OJ was associated with significant hyperplasia and hypertrophy of the pancreas in rats as shown by increased DNA and RNA contents of pancreatic tissue. Factors associated with pancreatic growth in OJ rats were further examined in isolated dispersed pancreatic acini from OJ rats and the data were compared with those for control rats. Studies with isolated dispersed acini from OJ rats showed that pancreatic growth was accompanied by significant increases in total cellular amylase content; however, amylase release (percentage of initial) in response to cholecystokinin octapeptide was significantly decreased in OJ rats compared to control rats. Total amylase output in response to 100 pM cholecystokinin (CCK) was higher in the OJ group when compared to the control group (8.6 U/mg protein versus 6.4 U/mg protein), as calculated from the total amylase content and percentage of amylase released. Receptor binding data showed that the capacity of CCK receptors in OJ rats was significantly lower when it was compared with control. In addition, plasma levels of CCK were significantly elevated in OJ rats when compared to controls. These results suggest that obstructive jaundice induces pancreatic growth that is associated with alteration of exocrine pancreatic function. Abnormally high levels of stored amylase in pancreatic acini may be implicated in the development of pancreatitis as often seen in obstructive jaundice patients.
authors.affiliation: Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock 72205.
authors.forename: A
authors.initials: A
authors.lastname: Tangoku
authors.forename: P
authors.initials: P
authors.lastname: Chowdhury
authors.forename: Y S
authors.initials: YS
authors.lastname: Huang
authors.forename: R
authors.initials: R
authors.lastname: Doi
authors.forename: G T
authors.initials: GT
authors.lastname: Blevins
authors.forename: C
authors.initials: C
authors.lastname: Eyiuche
authors.forename: D W
authors.initials: DW
authors.lastname: McKay
authors.forename: P L
authors.initials: PL
authors.lastname: Rayford
mesh_terms: D000681:Amylases / Q000378:metabolism; D000818:Animals; D001652:Bile Ducts / Q000601:surgery; D001663:Bilirubin / Q000097:blood; D002779:Cholestasis / Q000503:physiopathology*; D004247:DNA / Q000378:metabolism; D006965:Hyperplasia; D006984:Hypertrophy; D008026:Ligation; D008297:Male; D010179:Pancreas / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D012313:RNA / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012844:Sincalide / Q000494:pharmacology
chemical_list: D012313:RNA; D004247:DNA; D000681:Amylases; D012844:Sincalide; D001663:Bilirubin