Abstract

Rats are the most common objects of preclinical studies, which determines the relevance of studying fetal cardiomorphogenesis in rats using modern methods of morphological studies. The aim is to study the dynamics of markers of proliferation (Ki67), apoptosis (caspase 3), vascularization (CD31), and stromal remodeling (MMP2 and MMP9) of the left ventricular myocardium of Wistar rat fetuses. Material and methods. A histological, immunohistochemical and morphometric study of the rat heart left ventricle wall was carried out on the 18th, 19th, 20th, 21st and 22nd days of the prenatal period of ontogenesis. Results. From the 18th to the 22nd day of the prenatal period of ontogenesis in rats, a twofold increase in the thickness of the left ventricle lateral wall is observed, due to both proliferation and differentiation and an increase in the size of cardiomyocytes. Ki67-positive cardiomyocytes are diffusely localized in the wall of the left ventricle, their number increases on day 19 of the prenatal period of development and remains at a high level until the end of the prenatal period in rats. From the 18th to the 22nd day of the prenatal period of ontogeny in rats, single caspase 3-positive cardiomyocytes are detected in the left ventricle. The growth of the left ventricular myocardium in the fetal period in rats is accompanied by an adequate rate of vascularization. The vascularization and proliferation of cardiomyocytes are accompanied by remodeling of the myocardial stroma, with the highest intensity of MMP2- and MMP9-immune staining observed at the beginning of the fetal period of ontogeny in rats. Conclusion. The short duration of prenatal ontogenesis in rats determines the high dynamics of cardiomorphogenetic processes. In the fetal period of rat ontogenesis in the left ventricle of the heart, the proliferation of cardiomyocytes prevails over the intensity of apoptosis. The intensity of proliferation of cardiomyocytes of the left ventricle of rats is high up to the 22nd day of the prenatal period of ontogenesis.

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