Histological Features of the Hepatic and Pancreatic Structure of Female Rats in the Model of Biliary Pancreatitis with Hyperprolactinemia

Liver diseases accompanied by obstructive cholestasis (OC)often depend on sex. Prolactin hormone levels are often elevatedin a variety of hepatopancreatobiliary zone diseases, which is anadverse prognostic sign. To clarify the role of prolactin in thedevelopment of pancreatitis under OC conditions, structural changesin hepatic and pancreatic tissue female rats against the backgroundof hyperprolactinemia were investigated. The rats were divided intothe following experimental groups: group K—control animals; groupHyperPrl—animals with normal hepatic function against the backgroundof hyperprolactinemia; group BP—animals with biliary pancreatitisunder OC; group BPhyperPrl—animals with biliary pancreatitis underOC against the background of hyperprolactinemia. Hyperprolactinemiawas modeled by transplanting the donor’s pituitary gland under therecipient’s kidney capsule. Biliary pancreatitis was simulated witha ligation of the biliopancreatic duct 1 cm prior to its dischargeinto the duodenum, causing obstruction of the ducts of the splenicsegment of pancreas. After 14 days of operations, a biomaterialwas collected. The biochemical indicators of the blood serum confirmedthe development of OC and pancreatitis. The structure of the pancreaticparenchyma in the BP and BPhyperPrl groups was changed, especiallyin the splenic segment. In both groups, tubulo-insula and tubulo-acinarcomplexes, inflammatory infiltration, acinaro-ductal metaplasiawere found, which was accompanied by severe pancreatic parenchymafibrosis in the group BPhyperPrl. It is important to note that theduodenal segment of pancreas continued to compensate for pancreatitisdevelopment in the BP and BPhyperPrl groups. In the hepatic tissue,histological confirmation of the development of obstructive cholestasiswas shown in the BP and BPhyperPrl groups, with the loss of thebeam structure of hepatocytes and the development of pericellularfibrosis against the background of hyperprolactinemia. Thus, wefirst showed in our work that female rats with increased prolactin concentrationon the background of OC develop a heavier form of pancreatitis witha pronounced pancreatic fibrosis. This model of the developmentof biliary pancreatitis under OC can be used not only to study therole of prolactin in disruption of the pancreas, but also its participationin compensatory reactions to maintain the work of the exocrine partof the pancreas in this pathology.