title: Time-course changes in pancreatic laboratory and morphologic parameters in two different acute pancreatitis models in rats.
abstract: The aim of this work was to study in rats the temporal course of laboratory parameters and morphologic features in acute pancreatitis induced by cholecystokinin octapeptide (CCK-8) or by a closed duodenal loop. Pancreatitis was induced either with an overdose of CCK-8 (3 x 75 micrograms/kg at 1 h intervals) or by ligation of the duodenum on both sides of the bilio-pancreatic duct. The animals were examined at 0, 2, 4, 8, 16 and 24 h after AP induction. In CCK-8-induced acute pancreatitis, the pancreatic weight/body weight ratio (8.2 +/- 1.1 mg/g) and the amylase level (44.8 +/- 7.5 x 10(3) U/ml) were significantly increased vs. the controls (4.5 +/- 0.8 mg/g and 3.3 +/- 0.2 x 10(3) U/ml, respectively) 2 h after the intervention. The plasma CCK was significantly increased at 4 h (4.55 +/- 1.7 pM) and remained elevated thereafter. The tissue malonyldialdehyde concentration was significantly elevated at 8 h (0.28 +/- 0.07 mumol/mg pancreas) vs. the controls (0.20 +/- 0.02 mumol/mg pancreas). In closed duodenal loop-induced acute pancreatitis, the ratio pancreatic weight/body weight steadily increased during the study; it reached its maximum level at 24 h (7.1 +/- 0.5 mg/g) vs. the sham-operated control (4.8 +/- 0.9 mg/g). The serum amylase level was significantly elevated at 2 h (47.1 +/- 9.3 x 10(3) U/ml), and then decreased steadily. Plasma CCK values were significantly higher than the controls throughout the study. A significant increase in the tissue malonyldialdehyde concentration (0.94 +/- 0.15 mumol/mg vs. 0.20 +/- 0.01 mumol/mg pancreas) appeared at 4 h. Our data indicate that in CCK-8-induced acute pancreatitis the laboratory signs of pancreatitis are most expressed at 4 h, whereas the morphologic changes culminate 8 h, following the last CCK injection. In closed duodenal loop-induced acute pancreatitis, the histologic findings showed a progressive deterioration. Endogenous CCK and oxygen-derived free radicals seem to play a role in the pathogenesis of both types of acute pancreatitis.
authors.affiliation: First Department of Medicine, Albert Szent-Györgyi Medical University, Szeged, Hungary.
authors.forename: T
authors.initials: T
authors.lastname: Takács
authors.forename: L
authors.initials: L
authors.lastname: Czakó
authors.forename: K
authors.initials: K
authors.lastname: Jármay
authors.forename: P
authors.initials: P
authors.lastname: Hegyi
authors.forename: J
authors.initials: J
authors.lastname: Pozsár
authors.forename: E
authors.initials: E
authors.lastname: Marosi
authors.forename: A
authors.initials: A
authors.lastname: Pap
authors.forename: J
authors.initials: J
authors.lastname: Lonovics
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000818:Animals; D002766:Cholecystokinin / Q000097:blood*; D004195:Disease Models, Animal; D004380:Duodenal Obstruction; D015227:Lipid Peroxidation / Q000502:physiology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009929:Organ Size; D010195:Pancreatitis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D012844:Sincalide; D013997:Time Factors
chemical_list: D008315:Malondialdehyde; D002766:Cholecystokinin; D000681:Amylases; D012844:Sincalide