PATHOMORPHOLOGICAL FEATURES OF RAT LIVER EXPOSED TO MIXED HYPOXIA

• Main Authors: Sherstiuk S. O., Zotova A. B.
• Format: Article
• Language: English
• Published: Ukrainian Medical Stomatological Academy 2019-04-01
• Series: Вісник проблем біології і медицини
• Subjects: mixed hypoxia; rats; liver; postnatal period.
• Online Access: https://vpbm.com.ua/upload/2019-2-1/70-min.pdf

Perinatal pathology is one of the important problems in present-day medicine. The mechanism of its development is complex and caused by impaired fetoplacental circulation. According to the modern concepts, the antenatal and intrapartum hypoxia of fetus developing on the background of mothers pathology, occupies the leading place among the causes of perinatal pathology. The complexity of liver function development in the antenatal and intrapartum periods, immaturity of enzyme systems as well as continuing morphological differentiation of structural elements cause the high sensitivity of this organ to the various factors exposure on the part of the maternal organism. In this regard, the study of hypoxia effect on the postnatal state of children liver is the important task and requires experimental substantiation. The aim of the study was to identify the pathomorphological features of rat liver at different periods of postnatal ontogenesis, which were exposed to mixed hypoxia. The study material was rat liver tissue. The research included two groups: I group consisted of WAG rats born from females with physiological pregnancy and euthanized on 1, 14 and 35 days of postnatal ontogenesis; II group included rats of Black hood population developed in conditions of chronic antenatal hypoxia which was caused by the presence of arterial hypertension in maternal organism, exposed for 1 day of postnatal ontogenesis to highaltitude hypoxia and euthanized on 1, 14 and 35 days. The analysis of research data has identified the regular age-related increase in hepatocytes size in I group. In II group, with the increase in the duration of the experiment, the sizes of hepatocytes were significantly larger (p <0.05) compared to I group which was caused by dystrophic changes in the cells which, in our view, was not only due to age-related changes, but also to the effect of such damaging factor as hypoxia. The number of hepatocytes per field of view in rats of II group have been significantly (p <0.05) lower than those in I group at all periods of the experiment. The data of experiment have determined that mixed hypoxia led to the development of significant destructivedystrophic changes in the liver tissue of rats. The diameter of hepatocytes in descendants exposed to mixed hypoxia progressively increased on 1 (28.54 ± 0.64 ?m), 14 (32.78 ± 0.38 ?m) and 35 (42.39 ± 1.54 ?m) days after birth. The number of hepatocytes per field of view in rats of the group with mixed hypoxia progressively decreased on 1 (180.4 ± 4.12 cells), 14 (162.8 ± 4.30 cells) and 35 (114.3 ± 1.18 cells) days after birth. The ratio of the number of binuclear hepatocytes to the number of mononuclear hepatocytes in rats of group with the mixed hypoxia was progressively increasing on 1 (12.36 ± 0.007%), 14 (18.34 ± 0.008%) and 35 (21.34 ± 0.005%) days after birth. The histological examination of microsections has revealed that the expressed sclerotic changes in the rat liver of II group compared to group I were caused by aggressive damaging factor, namely, mixed hypoxia