Introduction. To date, there are limited opportunities to study the effects of congenital airway pathology in the experiment. To study the damage to body tissues in case of impaired airway ventilation, the author's version of artificial narrowing of the tracheal lumen by applying ligatures was used. The study of morphofunctional reactions and structural changes in organs and tissues of the body made it possible to identify and study pathogenetic and target tissue targets in order to develop tactics for the treatment of this pathology in newborns. Objective: to investigate the peculiarities of ultrastructural changes in the cells of the sensorimotor cortex of the cerebral hemispheres of experimental immature animals after modelling partial tracheal stenosis. Materials and methods. Ligature was applied to young rats at the level of the upper third of the trachea, which limited the tracheal lumen by about 25-30%. After modelling the pathology of the upper respiratory tract, the appearance of characteristic wheezing sounds was noted, this allowed us to consider the experimental intervention as an analogue of the stridor model in newborns. On day 7 and day 21 of the experiment, after surgery and removal of the previously applied ligature, the ultrastructure of the sensorimotor cortex of young animals was studied and, on this basis, variants of pharmacological protective and therapeutic effects and acceleration of cerebral rehabilitation in experimental animals were proposed. Results. The development of neurodystrophic processes and damage to cell ultrastructures and blood-brain barrier functions were established. After removal of the ligature from the trachea and elimination of the artificial compression effect of this factor on the airways of animals, the observed dynamics of pathological ultrastructural changes remained virtually unchanged, even after repeated surgical procedures. This indicates the need for the use of pharmacological agents and medical technologies to restore cytomembranes in cells of the central nervous system of different types under the influence of chronic hypoxia. Conclusions. Partial tracheal stenosis causes damage to the nerve cells of the cerebrocortex, and the removal of the ligature on day 7 of the stenosis modelling experiment did not affect any ultrastructural changes compared to the results obtained in the group of animals with chronic tracheal stenosis. The restoration of lung ventilation and the nature of the data revealed indicate the absence of significant recovery changes in the nerve and vascular cells of the brain. They indicate the need for urgent therapeutic and rehabilitation measures to accelerate the restoration of the structure and functions of cerebrocortical cells in the posthypoxic period.