Патоморфологічні особливості печінки нащадків, які зазнали впливу гострої постнатальної гіпоксії

Abstract

The purpose of the study was to identify pathomorphic features of rat liver at different stages of postnatal ontogenesis caused by acute postnatal hypoxia. Materials and methods. All animals were divided into two groups C (control) and APH (acute postnatal hypoxia). Group C included 33 WAG line rats born from females with physiological pregnancies whereas group APH included 37 WAG line rats. Healthy rats of group APH were exposed to "alpine hypoxia" immediately after birth. The rats in both research groups were withdrawn from the experiment on days 1, 14, and 35 after their birth. The research material was the liver of experimental animals of both groups obtained at autopsy. Results and discussion. Having analyzed the morphometric parameters of group C hepatocytes, it can be stated that in the process of formation and maturation of liver beams there is an increase in the size of hepatocytes, which indicates the morphological and functional maturation of the tissue. According to the value of NCI (nuclear cytoplasmic index) in group APH1 there was an increase in the diameter of hepatocytes due to an increase in cytoplasmic volume, which can be explained by the instantaneous response of hepatocytes to acute hypoxia, manifested by metabolic imbalance and cell swelling. It should be noted that after the cessation of acute hypoxia, the size of hepatocytes gradually normalizes (groups AHP2-3). A significant (p <0.05) decrease in the total number of hepatocytes due to their mononuclear forms was also observed in the liver of APH1-3 group rats. In group APH3, on the 35th day after birth, the restoration of the structural and functional integrity of the liver occurred due to an increase in the number of binuclear hepatocytes, and was manifested by nearly two-time-increase in their number. Conclusion. The simulated acute postnatal hypoxia of rat descendants from healthy mothers caused a failure of compensatory capabilities with a sharp suppression of morphofunctional activity of the liver on day 1 of the experiment. The diameter of hepatocytes of the descendants exposed to acute postnatal hypoxia was significantly larger on day 1 (25.52±2.5 μm), and gradually normalized on days 14 (27.11±2.8) and 35 (38.94±3, 1 μm) after birth. The number of hepatocytes in the field of view in rats of acute postnatal hypoxia group progressively decreased on days 1 (198.7±13.1 cells), 14 (170.2±11.8 cells) and 35 (152.5±13.8 cells) after birth. The ratio of the number of binuclear hepatocytes to the number of mononuclear hepatocytes in rats of acute postnatal hypoxia group progressively increased on days 1 (0.02±0.01), 14 (0.05±0.01) and 35 (0.10±0.01) after birth