Asadova T. A.

PATHOMORPHOLOGY

Scentific article

Abstract. 102 premature infants with perinatal hypoxic-ischemic CNS lesions from mothers with a burdened obstetric history aged from 1 day to 1 month of life were examined. Most of the children were born to mothers under the age of 35-72 (70.6%), the rest were over 35 – 30 (29.4%). Premature children of the male sex were 53 (52%), female – 49 (48%); residents of the city – 70 (68.7%), the village – 32 (31.3%). The examination of premature infants was carried out on days 1-3, 5-7, and again on days 10-14. The following research methods were used: clinical, morphofunctional immaturity parameters, anthropometric indicators, functional state of organs and systems. The gestational age (g/v) of infants was determined based on the mothers ‘ anamnesis and ultrasound results. Endothelial nitric oxide synthase (eNOS or NOS-3) was determined by enzyme immunoassay (ELISA). Studies were carried out: RN-diagnostics of the chest organs, NSG; Doppler studies of the vascular system ; EchoCG, ECG. Results. Cerebral ischemia (CI) of the first stage was detected in n=51; CI of the second stage in n=32; CI of the third stage in n=19 premature infants, respectively. To identify the role of vasoregulatory mechanisms in CNS damage, the nitric oxide synthase system was studied, in particular, the role of endothelial synthase (eNOS) in 71 premature infants, depending on g/v and the severity of CI. eNOS has been shown to play a leading role in the development of cerebral ischemia. It was revealed that the increased expression and activation of eNOS directly depends on the gestational age of the infant. The more pronounced the effect of hypoxia and ischemia, the more pronounced the violation of the ability of adequate function and structure of the endothelial cells of the brain vessels, which contributes to the occurrence of cerebral ischemia of varying severity, leading to serious consequences. Conclusions. In the pathogenesis of hypoxic ischemic encephalopathy, eNOS is the main indicator of the processes of endothelial dysfunction of the cerebral vessels, simultaneously reflecting both its cause and effect.

prematurity, pathology of the central nervous system, hypoxic lesion of the central nervous system, endothelial synthase eNOS.

1. Huseynova SA, Akhundova A, Panakhova N, Hasanov S, Ali-zade S. Endotelial Nitric Oxide Function and Tubular Injuri in Premature Infants. International Journal of Applied Science and Texnology. 2012;2(6):77-81.
2. Al’perina ON. Klinicheskie osobennosti i metody patogeneticheskoj korrekcii perinatal’nogo porazhenija central’noj nervnoj sistemy u nedonoshennyh detej s retinopatiej [dysertatsiia]. Ekaterinburg: Ural. gos. med. akad. 2011. 21 s. [in Russiаn].
3. Dolinina AF, Gromova LL, Kopylova ER. Ishody perinatal’nyh povrezhdenij central’noj nervnoj sistemy gipoksicheskogo geneza u nedonoshennyh detej. Zh. Pediatricheskij vestnik Juzhnogo Urala. 2014;1.2:44-47. [in Russiаn].
4. Pal’chik AB, Fedorova LA, Ponjatishin AE. Nevrologija nedonoshennyh detej. Moskva: MEDpress-inform; 2011. 352 s. [in Russiаn].
5. Baburamani AA, Hurling C, Stolp H, Sobotka K, Gressens P, Hagberg H, et al. Mitoxondrial Optic Atrophy (OPA) 1 Pracessing is Altered in Response to Neonatal Hypoxic-Ishemic Brain Injury. Int J Mol Sci. 2015 Sep 17;16(9):22509-26. DOI: 10.3390/ijms160922509.
6. Garry PS, Ezra M, Rowlanfd MJ, Westbrook J, Pattinson KTS. The role of the nitric oxide pathway in brain injury and its treatment- from bench to bedside. Exp Neurol. 2015;263:235-43. DOI: 10.1016/j.expneurol.2014.10. 017.
7. Van Iersse SH, Conraads VM, Van Craenenbroeck EM, Liu Y, Maas AIR, Parizel PM, et al. Endothelial dysfunction in acute brain injury and the development of cerebral ischemia. J Neurosci Res. 2015;93(6):866-72. DOI: 10.1002/jnr.23566.
8. Wong LF, Wilkes J, Korgenski K, Varner MW, Manuck TA. Risk factors associated with preterm birth after a prior term delivery. BJOG. 2016;123(11):1772-8. DOI: 10.1111/1471-0528.13683.

«Bulletin of problems biology and medicine» Issue 2 (160), 2021 year, 262-265 pages, index UDK UDC 616.8–007.1–053.31 (075.8): 575.174.015.3; :577.151

10.29254/2077-4214-2021-2-160-262-265