CLINICAL AND PATHOGENETIC FEATURES OF MICROCIRCULATORY CHANGES IN BRONCHOPULMONARY DISEASES IN CHILDREN

Abstract

Relevance. Inflammatory bronchopulmonary diseases in children, such as bronchitis, pneumonia, and bronchiolitis, remain among the most urgent problems in modern pediatrics. Microcirculatory dysfunction plays a central role in their pathogenesis. Impairment of the microcirculation not only disrupts alveolar gas exchange but also affects tissue trophic supply. Contemporary research highlights a close association between this dysfunction and the imbalance of inflammatory mediators — interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), and the anti-inflammatory cytokine interleukin-10 (IL-10). These mediators alter endothelial cell function, increase capillary wall permeability, cause degradation of the glycocalyx structure, and consequently lead to impaired microvascular perfusion. Objective. The aim of this study was to identify the main pathophysiological mechanisms of microcirculatory dysfunction in inflammatory bronchopulmonary diseases in children, to assess the relationship between the levels of inflammatory cytokines (IL-1β, IL-6, TNF-α, IL-8, IL-10) and microcirculatory parameters, and to determine their clinical significance as prognostic biomarkers. Materials and Methods. To evaluate the state of microcirculation in pediatric patients, a comprehensive set of instrumental and laboratory diagnostic methods was applied. Capillaroscopy was used to assess the morphofunctional state of nail-bed capillaries, pulse oximetry was employed to determine arterial oxygenation levels, and blood lactate concentration served as a marker of metabolic hypoxia. Additionally, hemostasiogram parameters and microperfusion indices were calculated. The levels of inflammatory mediators were determined by the enzyme-linked immunosorbent assay (ELISA), followed by statistical correlation analysis to examine interrelations between cytokine and microcirculatory indicators. Results and Discussion. The analysis revealed a significant increase in inflammatory cytokine levels among children with bronchopulmonary diseases, which contributed to the development of endothelial dysfunction. Increased capillary wall permeability, degradation of the glycocalyx, and enhanced interstitial edema led to a decrease in microcirculatory blood flow. These changes were accompanied by impaired blood rheology, reduced erythrocyte deformability, and microthrombus formation. A statistically significant positive correlation (r = 0.68–0.74; p < 0.01) was established between IL-6 and TNF-α levels, on the one hand, and lactate concentration and capillary perfusion indices, on the other. This relationship was found to be a reliable diagnostic biomarker for predicting severe courses of pneumonia and bronchiolitis. Particularly in young children, the morphofunctional and metabolic immaturity of adaptive mechanisms leads to rapid transition of microcirculatory disorders into a hypoxic-decompensatory stage. Conclusion. The obtained results confirm that microcirculatory dysfunction represents a key pathogenetic link in the development of inflammatory bronchopulmonary diseases in children. Early diagnosis and complex correction of these disorders can reduce disease severity, prevent hypoxic complications, and improve clinical outcomes. In the future, integrating microcirculatory markers, inflammatory cytokines, and oxidative stress indicators into a unified monitoring system may provide a basis for optimizing diagnostic and therapeutic strategies in pediatric practice.