Submicroscopic changes of secretory cardiomyocytes under the experimental hyperglycemia in rats of different age groups

S V Trach Rosolovska,Y Y Bodnar,Z M Nebesna,V V Kulbitska

doi:10.11603/bmbr.2706-6290.2021.4.12768

Abstract

Summary. Diabetes mellitus today is one of the most common diseases of humankind. One of the risk factors for heart disease in diabetes is chronic hyperglycemia, which causes cardiovascular disease and myocardial injury. Ultrastructural changes of endocrine cardiomyocytes of a heart in hyperglycemia in the experiment require more detailed study. The aim of the study – to establish submicroscopic changes of atrial myoendocrine cardiomyocytes under the conditions of modeling of experimental hyperglycemia in rats of different age groups. Materials and Methods. The study was performed on 24 outbreeding nonlinear adult male rats. Experimental hyperglycemia was simulated by a single intraperitoneal injection of streptozotocin (Sigma, USA). Animals were divided into two age groups: of pre-reproductive and reproductive age. For electron microscopic studies, sections 0.4–0.6 μm thick were made on an ultramicrotome, and were studied using an electron microscope PEM-125K. Results. Submicroscopic studies of the right and left atrial appendages (auricles of the heart) of the studied groups of animals after one month of experimental persistent hyperglycemia showed changes in the structure of almost all organelles of endocrine cardiomyocytes. Changes in secretory cells of the right and left atrial appendages after two months of experimental persistent hyperglycemia showed an increase in destructive changes in the structural components of cells, which were more pronounced in the group of animals of pre-reproductive age. The diffuse collagenization of the stroma was a typical sign of ultrastructural changes in the atrial appendages after three months of experimental persistent hyperglycemia. Conclusions. At experimental steady hyperglycemia at animals of different age groups stereotypical ultrastructural reorganization of secretory cardiomyocytes of right and left atrial appendages with development of compensatory-adaptive and destructive changes is noted. In the dynamics of the experiment there is an increase in destructive phenomena, the severity of which is higher in the group of rats of pre-reproductive age.

Highlights

Diabetes mellitus (DM) is currently one of the most common diseases of humankind, leading to disability and mortality in many countries around the world
Changes in secretory cells of the right and left atrial appendages after two months of experimental persistent hyperglycemia showed an increase in destructive changes in the structural components of cells, which were more pronounced in the group of animals of pre-reproductive age
The pathomorphology of structural components of the organ in experimental hyperglycemia is described in details in the scientific literature [16, 17], but more attention has been paid to the structure of the myocardium, while ultrastructural changes of endocrine cardiomyocytes in the experimental hyperclycemia require more detailed study and in the future will predict the pathogenesis of heart disease in diabetes

Summary

Introduction

Diabetes mellitus (DM) is currently one of the most common diseases of humankind, leading to disability and mortality in many countries around the world. One of the most important risk factors for heart disease in DM is chronic hyperglycemia, which causes cardiovascular disease and contributes to myocardial injury [4–8], and the degree of structural and functional changes in the components of the organ depends on various factors, including neurohumoral regulation [9, 10]. The pathomorphology of structural components of the organ in experimental hyperglycemia is described in details in the scientific literature [16, 17], but more attention has been paid to the structure of the myocardium, while ultrastructural changes of endocrine cardiomyocytes in the experimental hyperclycemia require more detailed study and in the future will predict the pathogenesis of heart disease in diabetes

Methods

Results

Conclusion