Abstract
Introduction. The nature of damage to the body in COVID-19 is of major interest; however, the cardiac mechanisms of death have not been fully studied. The causes of deaths from CVDs require a search for heart failure mechanisms, one of which is an increased burden on the right ventricle due to changes in the affected pulmonary blood vessels. The aim was to assess changes in hydrodynamic resistance in the pulmonary microvasculature in accordance with the variant of the prevailing pathological process in them and the COVID-19 phase. Materials and methods. We performed clinical and morphological analyses of 20 lethal cases with the primary diagnosis of coronavirus infection caused by SARS-CoV-2. We used morphometry to measure the internal diameter of arterioles and venules, the specific capillary area (SCA), and the total radius of the capillary bed. The vascular radius formed the basis for calculating the hydrodynamic resistance in the sections of the microvasculature of the pulmonary circulation. Results. The exudation phase is accompanied by an increased lumen of arterioles and venules against the background of a decreased specific density of the capillary bed. In the early proliferation phase, the capillary bed reduces significantly, and dilatation is replaced by spastic manifestations in arterioles and, to a lesser extent, in venules. The late proliferative phase has similar reduction levels in the total capillary radius and the degree of vasoconstriction of arterioles especially in the zone of increased airiness and grown connective tissue. Conclusion. The reduced capillary bed is of primary importance in increasing the calculated hydrodynamic resistance in the lung tissue during COVID-19. The growth in the average calculated hydrodynamic resistance in the lung tissue occurs to a greater extent during the proliferative phases (early and late) of COVID-19 infection. Keywords: COVID-19, SARS-CoV-2, lungs, vessels
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