Dynamics of Morphological Transformation of Myocardial Tissue Components Under the Influence of Acute Prenatal Hypoxia in Late Gestation

The critical importance of late gestation for cardiogenesis means that prenatal hypoxia is a leading factor in the development of congenital cardiomyopathies and heart failure in adulthood. The aim was to investigate the dynamics of morphological transformation of myocardial tissue components in rat embryos and foetuses at late stages of gestation under the influence of acute prenatal hypoxia. Material and methods. The experimental part of the study was carried out on 35 female white laboratory rats using morphometry and light microscopy of the myocardium of the right and left ventricles of embryos and foetuses at 15, 16, 18 and 20 days of intrauterine development. Results. It has been established that acute prenatal hypoxia (APH) on the 13th day of rat embryogenesis disrupts ventricular trabeculation due to a delay in the reduction of the cardiac gel, myoblast necrosis and excessive cell proliferation during the epithelial-mesenchymal transition. By the 15th day, trabecular oedema persists, uneven clusters of cardiomyoblasts develop, and the migration of epicardial derivatives is inhibited against a background of hypervascularisation of the compact myocardium. From the 16th day (following the anastomosis of the coronary bed with the aorta), despite the subsiding of hypoxic-inflammatory processes, a slowing of myocardial compaction is observed, with the spongy structure of the myocardium persisting for a prolonged period, accompanied by a disproportion in haemocapillary distribution and the activation of endothelial cell apoptosis. Before birth, the consequences of HPG manifest as a redistribution of vascular density: the numerical density of endothelial cells increases significantly in the compact myocardium of the left ventricle (by 25.8 per cent), the right ventricle (by 25.1 per cent) and the right atrium (by 32.8 per cent), but decreases significantly in the trabecular myocardium of both ventricles (by 38.0 % and 39.4 % respectively; p<0.05). Conclusions. Acute prenatal hypoxia leads to a delay in ventricular myocardial compaction, impaired trabeculation, and a statistically significant imbalance in endothelial cell density between the compact and trabecular layers prior to birth.