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Published on: July 14, 2021
Rat Left Ventricular Cardiomyocytes Characterization in the Process of Postinfarction Myocardial Remodeling
Ekaterina V Baidyuk1, Galina A Sakuta1, Mikhail L Vorobev1
1Laboratory of Cell Pathology, Institute of Cytology of the Russian Academy of Sciences, Saint-Petersburg, Russia.
Insights
Myocardial infarction causes lasting changes in heart cell size and mass, but not ploidy. Heart cell numbers do not recover after infarction, impacting cardiovascular health.
Area of Science:
- Cardiovascular Science
- Cell Biology
- Pathology
Background:
- Ischemic heart lesions, including myocardial infarction, are leading causes of cardiovascular mortality.
- Understanding myocardial changes post-infarction is crucial for improving patient outcomes.
- Previous research highlights the need to investigate cellular dynamics in early and late infarction stages.
Purpose of the Study:
- To investigate changes in rat cardiomyocyte (CMC) ploidy, hypertrophy, hyperplasia, and ultrastructure after experimental myocardial infarction.
- To analyze these cellular changes at 2, 6, and 26 weeks post-infarction.
Main Methods:
- Experimental myocardial infarction induced by permanent ligation of the left coronary artery in rats.
- Cell ploidy assessed using cytofluorimetry.
- Cell size and dry mass measured by interference microscopy.
- Ultrastructure analyzed via electron microscopy.
- Cell counting performed to assess cardiomyocyte numbers.
Main Results:
- No significant differences in cardiomyocyte ploidy were observed between control and infarcted groups at any time point.
- Significant alterations in cardiomyocyte size and dry mass were detected: decreased at 2 weeks, increased at 6 weeks, and localized increase in the peri-infarction zone at 26 weeks.
- Electron microscopy revealed sarcomere structure disruption. Cardiomyocyte numbers were reduced post-infarction and did not recover during remodeling.
Conclusions:
- Experimental myocardial infarction leads to substantial changes in cardiomyocyte size and mass, but not ploidy.
- The loss of cardiomyocytes following infarction is permanent and not restored through the remodeling process.
- These findings underscore the persistent cellular damage and remodeling challenges after myocardial infarction.
Abstract:
Ischemic lesions of the heart, including myocardial infarction, are the most common pathologies of human cardiovascular system. Despite all the research and achievements of medicine in this field, the mortality from this disease remains heavy. Therefore, studying of processes occurring in the myocardium in the early and late postinfarction periods remains important. Rat left ventricular cardiomyocyte (CMC) ploidy, hypertrophy, hyperplasia, and ultrastructure were investigated in 2, 6, and 26 weeks after experimental myocardial infarction, caused by permanent ligation of left coronary artery. Cytofluorimetric study of CMC ploidy revealed no difference between normal, sham-operated, and infarcted animals for all the tested stages. However, interference microscopy indicated significant changes in cells size. CMC dry mass of infarcted rats in 2 weeks after surgery was 1.5 times lower than in control and sham operated groups. Electron microscopy analysis of CMC revealed disruption of sarcomere structure. However, in 6 weeks after surgery CMC dry mass was 1.6 times higher than in control. In 26 weeks after myocardial infarction CMC dry mass exceeded control only in peri-infarction zone. Cell counting showed that the number of left ventricular CMC, reduced as a result of myocardial infarction, was not restored during myocardial remodeling. © 2019 International Society for Advancement of Cytometry.
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