FEATURES OF CHANGES IN THE SYNTHESIS AND QUALITY OF LUNG SURFACTANT AFTER CHRONIC PHYSICAL EXERTION

Abstract

The article describes a research study that investigates changes in the ventilation-perfusion function of the lungs due to prolonged physical exertion. The study was conducted on male white laboratory rats aged between 5-10 months and weighing 120.0-140.0 g, with a total of 25 rats used, 10 of which were of the same age group. The study utilized lung tissue of the animals, and anatomical, histological, electronhistochemical, and ultramicroscopic methods were employed to comprehensively investigate the modal changes that occur after exposure to chronic prolonged physical load in the respiratory section of the lungs. During the presentation, a Tesla BS 500 electron microscope was used, and the static Microsoft Excel LL XP program was used on a "Sony Vaio" personal computer. Differences in the compared groups were considered significant (p<0.05). The study findings indicate that prolonged physical activity disrupts the synthesis and utilization of surfactant in the alveoli of the lungs, increases the number of areas of distelectasis, and leads to hypoventilation acidosis. Furthermore, changes in the ultrastructure of alveolar macrophages during prolonged physical activity indicate an increase in the number of free macrophages on the background of an increase in the "absorbing" effect of their osmiophilic plates, leading to a decrease in the amount and intensity of the surfactant. A long-term regimen of physical load causes violations in the structures of the aero-hematic barrier and alveolar epithelium, as well as in the synthesis and utilization of surfactant. The data of electron-histochemical reactions indicate the instability of the components of the aero-hematic membrane and the processes of synthesis and utilization of the surfactant. The results of the study reveal that an increase in the body's oxygen demand under conditions of increased physical activity leads to increased ventilation of the lungs, hypoxia, and hypercapnia. In response to respiratory hypoxia, hypertension develops in the pulmonary circulation, causing focal lesions of the right ventricle. The data on lung and myocardial injury are significant for clarifying the structure of the model of long-term physical load.