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 The rats in both research groups were withdrawn from the experiment on days 1, 14, and 35 after their birth.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

Aim. The article is devoted to the study of pathomorphological features of fetal liver and newborns affected by chronic intrauterine hypoxia, which developed against maternal hypertension. Materials and methods. The studies were performed on liver preparations of 18 fetuses and newborns from mothers with physiological pregnancy (group I) and 36 fetuses and newborns from mothers with stage II hypertension (group II) at the age of 37 weeks of gestation - the 1st day of postnatal life. In each case, three fragments were excised from the liver, and then the material was fixed in 10 % formalin solution. Formalin-fixed tissue compaction was achieved by conducting, through alcohols, increasing concentrations, celloidin, chloroform, and paraffin embedding. From the prepared blocks for serial color serial sections with a thickness of 4–5 microns were prepared. Micropreparations were stained with hematoxylin and eosin, picrofuxin by the van Gizon method, and by the Mallory method. The diameter of the hepatocytes and their nuclei, NPP, were calculated, and the number of single and double-nucleated hepatocytes was calculated. The material was studied on an «Olympus BX-41» microscope with a digital camera. Results. The results of our study showed that the influence of chronic intrauterine hypoxia on the background of stage II hypertension led to the development of destructive-dystrophic changes in the liver tissue of the fetus and newborn. Structural and functional disorders, in turn, led to the activation of cellular regeneration mechanisms. In group II, the recovery of structural and functional integrity of the liver occurred due to an increase in the number of double-nucleated hepatocytes and manifested by an increase in their number almost 2-fold. Conclusions. During the study of pathomorphological features of fetal liver and newborns it was found that stage II hypertension in the mother leads to the development of significant destructive-dystrophic changes in the tissue of fetal liver and newborns. The diameter of hepatocytes of fetuses and newborns of group II was significantly increased compared with group I (24.3 ± 2.4 μm and 18.71 ± 2.8 μm, respectively). The number of hepatocytes in the field of view in the fetuses and newborns of group II significantly decreased compared with group I (214.8 ± 22.80 and 268.1 ± 24.11 cells, respectively). The ratio of the number of binucleate hepatocytes to the number of binucleate hepatocytes in fetuses and newborns of group II compared to group I increased 2.5 times (0.08 ± 0.02 and 0.03 ± 0.02, respectively).