Myocardial remodelling involves structural and functional changes in the heart, potentially leading to heart failure. The deoxycorticosterone acetate (DOCA)/salt model is a widely used experimental approach to study hypertension-induced cardiac remodelling. It allows to investigate the mechanisms underlying myocardial fibrosis and hypertrophy, which are key contributors to impaired cardiac function. In this study, myocardial remodelling in rat deoxycorticosterone acetate/salt model was examined over a three-week period. The experiment involved 11 male Sprague-Dawley rats, divided into two groups: fibrosis (n=6) and control (n=5). Myocardial remodelling was induced in the fibrosis group through unilateral nephrectomy, deoxyco-rticosterone acetate administration, and increased salt intake. The results revealed significant structural changes, including increased left ventricular wall thickness, myocardial fractional volume, and development of myocardial fibrosis. Despite these changes, left ventricular ejection fraction was preserved and even increased. ECG analysis showed significant prolongation of the PR interval and widening of the QRS complex in the fibrosis group, indicating disrupted atrioventricular and ventricular conduction, likely due to fibrosis and hypertrophy. Correlation analysis suggested a potential relationship between QRS duration and myocardial hypertrophy, although no significant correlations were found among other ECG parameters and structural changes detected by MRI. The study highlights the advantage of the DOCA/salt model in exploring the impact of myocardial remodelling on electrophysiological properties. Notably, this study is among the first to show that early myocardial remodelling in this model is accompanied by distinct electrophysiological changes, suggesting that advanced methods combined with established animal models can open new opportunities for research in this field. Key words Myocardial fibrosis, Remodelling, Animal model, DOCA-salt, Magnetic resonance imaging.
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http://dx.doi.org/10.33549/physiolres.935512 | DOI Listing |
Introduction: To determine the effects of atorvastatin on cardiac function and hemodynamics and to investigate its functional mechanism on cardiac fibrosis in acute myocardial infarction (AMI) rats.
Methods: Cardiac functions and hemodynamic changes were evaluated in each group on day 28. Quantitative reverse transcription-polymerase chain reaction, Western blot, and immunohistochemistry were performed to detect the expression of notch1, transforming growth factor-β (TGF-β), Smad2, Smad7, as well as myocardial fibrosis factors (i.
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