Affiliation:
1. IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY, IVANO-FRANKIVSK, UKRAINE
Abstract
Aim: To study the ultrastructural remodeling of atrial myoendocrine cells (AMC) of the atrial myocardium in streptozotocin-induced diabetes (SID) under chronic immobilization stress (CIS).
Materials and methods: 40 sexually mature white male rats (body weight 150-180 g) were included in the study. Four groups were formed: group 1 – animals with comorbid pathology (SID and CIS), group 2 – animals with SID, group 3 – animals with CIS, group 4 – intact animals.
Results: On the 14th day of the development of SID and CIS, an increase in the functional activity of AMC is noted, which is confirmed by hyperplasia and hypertrophy of the protein-synthesizing apparatus, an increase in the volume density of secretory granules (SG), especially diffusing ones, and indicates enhanced release of atrial natriuretic peptide (ANP) from cells during the experiment. On the 56th day of the experiment, in groups 1 and 2 of , destructive changes in AMC were noted, such as vacuolar and balloon dystrophy, colliquative and partial necrosis. At the same time, the functional activity of AMC of different regions of the myocardium significantly. In animals with CIS, the volume density of young and diffusing SG in AMC is decreased.
Conclusions: Therefore, in the early stages of the development of SID and CIS, an increase in the morpho-functional activity of AMC is noted. The long course of SID and its combination with CIS lead to destructive changes in AMC and to decrease in their secretory activity.
Reference24 articles.
1. 1. Saeedi P, Petersohn I, Salpea P et al. Global and regional diabetes prevalence estimates for 2019 and projections for 2030 and 2045: Results from the International Diabetes Federation Diabetes Atlas, 9th edition. Diabetes Research and Clinical Practice. 2019;157:107-108. doi: 10.1016/j.diabres.2019.107843.
2. 2. Wang M, Li Y, Li S, Lv J. Endothelial Dysfunction and Diabetic Cardiomyopathy. Front Endocrinol (Lausanne). 2022;13:851941. doi: 10.3389/fendo. 2022.851941.
3. 3. Packer M. Differential Pathophysiological Mechanisms in Heart Failure with a Reduced or Preserved Ejection Fraction in Diabetes. JACC Heart Fail. 2021;9(8):535-549. doi: 10.1016/j.jchf.2021.05.019.
4. 4. Radermecker RP, Philips JC, Jandrain B. Blood glucose control and cardiovascular disease in patients with type 2 diabetes. Rev. Med. Liege. 2008; 63 (7- 8): 511 – 518.
5. 5. Trachanas K, Sideris S, Aggeli С et al. Diabetic Cardiomyopathy: From Pathophysiology to Treatment. Hellenic J Cardiol. 2014; 55(5): 411-421.