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 elevated in a variety of hepatopancreatobiliary zone diseases, which is an adverse prognostic sign. To clarify the role of prolactin in the development of pancreatitis under OC conditions, structural changes in hepatic and pancreatic tissue female rats against the background of hyperprolactinemia were investigated. The rats were divided into the following experimental groups: group K—control animals; group HyperPrl—animals with normal hepatic function against the background of hyperprolactinemia; group BP—animals with biliary pancreatitis under OC; group BPhyperPrl—animals with biliary pancreatitis under OC against the background of hyperprolactinemia. Hyperprolactinemia was modeled by transplanting the donor’s pituitary gland under the recipient’s kidney capsule. Biliary pancreatitis was simulated with a ligation of the biliopancreatic duct 1 cm prior to its discharge into the duodenum, causing obstruction of the ducts of the splenic segment of pancreas. After 14 days of operations, a biomaterial was collected. The biochemical indicators of the blood serum confirmed the development of OC and pancreatitis. The structure of the pancreatic parenchyma in the BP and BPhyperPrl groups was changed, especially in the splenic segment. In both groups, tubulo-insula and tubulo-acinar complexes, inflammatory infiltration, acinaro-ductal metaplasia were found, which was accompanied by severe pancreatic parenchyma fibrosis in the group BPhyperPrl. It is important to note that the duodenal segment of pancreas continued to compensate for pancreatitis development in the BP and BPhyperPrl groups. In the hepatic tissue, histological confirmation of the development of obstructive cholestasis was shown in the BP and BPhyperPrl groups, with the loss of the beam structure of hepatocytes and the development of pericellular fibrosis against the background of hyperprolactinemia. Thus, we first showed in our work that female rats with increased prolactin concentration on the background of OC develop a heavier form of pancreatitis with a pronounced pancreatic fibrosis. This model of the development of biliary pancreatitis under OC can be used not only to study the role of prolactin in disruption of the pancreas, but also its participation in compensatory reactions to maintain the work of the exocrine part of the pancreas in this pathology.