The thesis is devoted to the research in some pathological-anatomical alterations of fetuses' and newborns' in the case of prenatal hypoxia caused by mother's hypertensive disease. Owing to the research it has been proved that mother's HT leads to abnormalities in the development, formation and maturation of fetuses' and newborns' hepatobiliary system. During our research the main cause of mature fetuses' and newborns' death was hypoxia and asphyxia in deliveries (58,4% in 2012 and 62,8% in 2017). The analysis of archive materials (2012-2017) has shown that the percentage of pregnancies with hypertensive disease equaled 5,61%. This research is based on 54 clinical and 117 experimental liver cases. Clinical material was divided into two groups: control or CG (fetuses and newborns with 37-40 weeks' gestation from healthy mothers according to the prenatal records) with 18 observations and the study group or HT (fetuses and newborns from mothers whose pregnancy was complicated by GC II stage). The group "HT" included 36 observations. An experimental study was conducted on pregnant female rats of WAG and SHR lines (a line of laboratory rats with genetically determined primary (essential) arterial hypertension and without any other related somatic diseases) at the age of 10-11 months and their descendants of different age in both sexes. SHR line was used in this work for CPH group (chronic prenatal hypoxia). WAG rat line is a line of somatic healthy lab rats for group C (Control) and group APH (acute postnatal hypoxia). In total, 36 sexually mature female rats weighing 180-220 g and 18 mature males were used to create pairs, from which 117 descendants were taken, which were withdrawn from the experiment in different periods (1, 14 and 35 days) depending on the study group and tasks set. It has been determined that the maternal HT is a risk factor of a child being born with the deficit of height and weight. It has been established that with maternal HT the increase in relative liver mass of fetuses and newborns has been registered more frequently due to the parenchyma volume decrease (60,2±4.5% compared to the control group 26,9±6,4%).With maternal HT in fetuses' and newborns' liver a significant drop of hepatocytes general number has been registered (214,8±22,80 cells) as well as a significant increase of their binucleated forms (16,2±1,8 cells) compared to the control group (268,1±24,1 and 8,2±1,1 cells respectively). It was established that the sclerotic processes of the stromal-vascular component of fetuses' and newborns' liver caused by maternal HT occur due to excessive proliferation of fibronectin (10.5±1.5% compared with the control group 7.5±1.2%) and collagen I and III types (13,8±2,1 and 13,2±1,9% compared with the control group 9,6±1,4 and 9,8±1,6% respectively). Maternal arterial hypertension has a negative impact on the morphological state of the hepatobiliary system of the fetus and newborns, which leads to severe parenchymal losses, fibrosis, and fatty liver hepatosis in the child.
