ISSN 2415-3060 (print), ISSN 2522-4972 (online)
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УЖМБС 2021, 6(2): 51–57
https://doi.org/10.26693/jmbs06.02.051
Experimental Medicine and Morphology

Pathomorphic Features of the Liver of Descendants Caused by Acute Postnatal Hypoxia

Sherstiuk S. O., Zotova А. B., Khramova Т. О., Sherstiuk L. L., Luhovykh V. D.
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 The rats in both research groups were withdrawn from the experiment on days 1, 14, and 35 after their birth.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

Keywords: acute postnatal hypoxia, rats, liver, postnatal period

Full text: PDF (Ukr) 442K

References
  1. Perepelitsa SA, Golubev AM, Moroz VV, Alekseeva SV. Prichinyi ostroy intranatalnoy i postnatalnoy gipoksii u novorojdennyih [The cause of acute intrapartum and postnatal hypoxia in newborns]. Obschaya reanimatologiya. 2012; 8(6): 17-22. [Russian]. https://doi.org/10.15360/1813-9779-2012-6-17
  2. Gunin AG, Samoylova AV, Demakov AB. Sistema otsenki riska estestvennyih rodov dlya ploda i novorojdennogo [System for assessing the risk of natural childbirth for the fetus and newborn]. Problemyi reproduktsii. 2012; 2: 90-92. [Russian]
  3. Ignatko IV, Kardanova MA, Tolkach YuI. Dekompensirovannaya platsentarnaya nedostatochnost i kriticheskoe sostoyanie ploda [Decompensated placental insufficiency and critical condition of the fetus]. Voprosyi ginekologii, akusherstva i perinatologii. 2015; 14(5): 36-46. [Russian]
  4. Yanko RV, Berezovskiy VA, Chaka EG, Levashov MI, Plotnikova LN, Litovka IG. Morfofunktsionalnaya harakteristika gepatotsitov normotenzivnyih i gipertenzivnyih kryis posle vozdeystviya preryivistoy normobaricheskoy gipoksii [Morphofunctional characteristics of hepatocytes in normotensive and hypertensive rats after exposure to intermittent normobaric hypoxia]. Regulatory Mechanisms in Biosystems. 2017; 8: 265-270. [Russian]. https://doi.org/10.15421/021741
  5. Kuznecov PA, Kozlov PV. Gipoksiya ploda i asfiksiya novorozhdennogo [Fetal hypoxia and newborn asphyxia]. Lechebnoe delo. 2017; 4: 9-15. [Russian]
  6. Znamenska TK. Gipoksiya ploda ta asfiksiya novonarodzhenogo [Fetal hypoxia and asphyxia of the newborn]. K; 2010. 463 p. [Russian]
  7. Sargosh O, Chetverikova O, Belikova I. Sravnitelnyj analiz dinamiki pokazatelej sostojanija zdorovja detej shkolnogo vozrasta Ukrainy v sovremennyh uslovijah [Comparative analysis of the dynamics of indicators of the health status of schoolchildren in Ukraine in modern conditions]. Wiadomości Lekarskie. 2017; 70(3): 462-5. [Russian]
  8. Vlassaks E, Nikiforou M, Strackx E. Acute and chronic immunomodulatory changes in rat liver after fetal and perinatal asphyxia. J Dev Orig Health Dis. 2014; 5(2): 98-108. PMid: 24847696. https://doi.org/10.1017/S2040174413000561
  9. Vonkova B, Blahakova I, Hruban L, Janku P, Pospisilova S. MicroRNA-210 expression during childbirth and postpartum as a potential biomarker of acute fetal hypoxia. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2019; 163(3): 259-64. PMid: 30565568. https://doi.org/10.5507/bp.2018.075
  10. Shevchenko LI, Znamenskaja TK, Rozova EV. Vlijanie gipoksicheskih sostojanij razlichnogo geneza na razvitie ploda i techenie rannego neonatal'nogo perioda u novorozhdennyh [Influence of hypoxic conditions of various origins on the development of the fetus and the course of the early neonatal period in newborns]. Neonatology, surgery and perinatal medicine. 2011; 1(1): 113-18. [Russian]
  11. Zotova AB. Vplyv khronichnoi vnutrishnoutrobnoi hipoksii na morfolohichni osoblyvosti pechinky v rannomu postnatalnomu periodi [Infusion of chronic intrauterine hypoxia on morpholonic features of the liver in the early postnatal period]. Abstr. PhDr. (Med.). Kh; 2019. 22 s. [Ukrainian]
  12. Buznickaya EV. Sovremennye vozmozhnosti neinvazivnoj diagnostiki fibroza pri zhirovoj bolezni pecheni u detej i podrostkov s ozhireniem [Modern possibilities of non-invasive diagnosis of fibrosis in fatty liver disease in obese children and adolescents]. Suchasna gastroenterologiya. 2014; 6 (80): 19–24. [Russian]
  13. Cienfuegos JA, Rotellar F, Baixauli J. Liver regeneration – the best kept secret. A model of tissue injury response. Rev Esp Enferm Dig. 2014; 106(3): 171–94.
  14. Lyzikov AN, Skuratov AG, Osipov ВВ. Mehanizmy regeneracii pecheni v norme i pri patologii [Mechanisms of liver regeneration in health and disease]. Problemy zdorovya i ekologii. 2015; 2: 4–9. [Russian]
  15. Duncan AW, Taylor MH, Hickey RD, Hanlon Newell AE, Lenzi ML, Olson SB, et al. The ploidy conveyor of mature hepatocytes as a source of genetic variation. Nature. 2010; 467(7316): 707–710. PMid: 20861837. PMCid: PMC2967727. https://doi.org/10.1038/nature09414
  16. Romanova LP, Malyshev II. Rol’ dvujadernyh gepatocitov v regeneracii pecheni posle mehanicheskoj travmy v rannem ontogeneze u krys. Vestnik Chuvashskogo Universiteta. 2011; 3: 398–402.