Surgical treatment of chronic malignant diseases of the biliopancratoduodenal area remains the most difficult problem of oncology and abdominal surgery, as evidenced by low resectability, high operative risk and unsatisfactory short-term and long-term results. Today, despite the increased interest of researchers in the problem of surgical treatment of patients with tumors of the distal common bile duct and pancreatic head, the pathogenesis remains insufficiently studied, namely the role of liver and kidney dysfunction (hepatorenal syndrome) in the development of complications due to structural metabolic disorders in the organs. In this regard, there is a need to further refine the development of algorithms for surgical interventions using minimally invasive antegrade and transpapillary interventions in the performance of radical and conditionally radical, as well as palliative interventions. The pathophysiological mechanisms of hepatorenal syndrome development, markers of its early diagnosis at the pre-clinical stage of development, as well as differentiated approaches to the treatment of patients to prevent the development of multiorgan disorders and improve treatment outcomes in patients with blastomatous mechanical jaundice also need to be clarified.
The experimental part of the work is devoted to clarifying the mechanisms of development of acute renal damage in rats with experimental acute mechanical jaundice, which was modeled by ligation of the common bile duct. Animals were divided into three groups: I – control (5 rats); ІІ (10 rats), in which the duration of mechanical jaundice was 3 days and ІІІ (10 rats), in which the duration of jaundice was 7 days. In cultures of liver and kidney cells of animals studied the secondary products of lipopreoxidation, hypoxia and evaluated the destruction of membranes by changes in phospholipid composition of cells. Nitrogen metabolites were studied in serum. Kidney Injury Molecule-1 (KIM-1) molecules were determined as a marker of acute renal damage in serum and kidney tissues.
In the course of experimental studies, it was found that on the 3rd day of modeling mechanical jaundice there is an acute liver injury, which is accompanied by membrane destabilizing processes in its tissue structures. Violation of the lipid composition of membranes occurs due to intensification in tissue structures of lipid peroxidation, which was expressed in an increase in tissue MD by 24,9 and 169,6% (p < 0,05) and tissue phospholipase A2 activity by 54,9 % and 134,5% (p <0,05 and decreased SOD activity 51,3 and 70,1 % (p < 0,05) in animals of groups II and III, progression of hypoxia, increase in lactate by 12,9 %, and 94,8 % (p <0,05) according to the terms of the study. In the tissues of the kidneys on the 3rd day of the experiment begin membrane destabilizing phenomena, but during this period the rates of azotemia increase insignificantly. KIM-1 protein, which serves as an early marker of renal damage in laboratory animals in the formation of hepatorenal syndrome in acute mechanical jaundice. against the background of microcirculation disorders, tissue hypoxia and activation of oxidative cell damage, which contributes to the development of membrane destabilizing processes in kidney tissue.
