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Updated: Jun 4, 2026
A Murine Model of Pressure Overload-Induced Right Ventricular Hypertrophy and Failure by Pulmonary Trunk Banding
Published on: June 14, 2024
Mechanism of pressure-overload right ventricular hypertrophy in infant rabbits
Sachito Minegishi1, Kazuo Kitahori, Arata Murakami
1Department of Cardiothoracic Surgery, The University of Tokyo, Tokyo, Japan.
Insights
Pressure-overload right ventricular hypertrophy, a risk in congenital heart disease, develops through cardiomyocyte apoptosis and fibrosis. This study reveals the mechanism in an infant rabbit model, offering insights into right ventricular heart failure progression.
Area of Science:
- Cardiovascular Science
- Pediatric Cardiology
- Pathophysiology
Background:
- Pressure-overload right ventricular hypertrophy is a known risk in congenital heart diseases like tetralogy of Fallot.
- The precise mechanisms underlying its development remain unclear.
Purpose of the Study:
- To investigate the developmental mechanism of pressure-overload right ventricular hypertrophy and subsequent heart failure.
- To elucidate the role of cardiomyocyte apoptosis and fibrosis in this process.
Main Methods:
- Induction of pressure-overload right ventricular hypertrophy in infant rabbits via pulmonary artery banding.
- Serial echocardiography to assess right ventricular function and dimensions.
- Histological and molecular analyses (TUNEL staining, Western blotting, Masson's trichrome stain) to evaluate cardiomyocyte apoptosis and fibrosis.
Main Results:
- Pulmonary artery banding successfully induced right ventricular hypertrophy and dysfunction.
- Right ventricular contraction and diastolic function decreased starting at 3 weeks post-surgery.
- Increased cardiomyocyte apoptosis was observed from 4 weeks, and fibrosis developed by 8 weeks post-surgery.
Conclusions:
- Pressure-overload in the right ventricle leads to disorder, hypertrophy, and fibrosis.
- Right ventricular cardiomyocyte apoptosis is implicated in the progression of pressure-overload induced hypertrophy.
- This infant rabbit model provides novel insights into the mechanisms of right ventricular hypertrophy development.
Abstract:
Although pressure-overload right ventricular hypertrophy is a long-term risk in some congenital heart diseases such as tetralogy of Fallot, how it develops is unclear. The aim of this study was to investigate the mechanism of development of this right ventricular heart failure.Pulmonary artery banding in 10-day-old rabbits induced pressure-overload right ventricular hypertrophy as they grew. Comparisons were made with age-matched sham controls (n = 24 per group). In weekly serial echocardiography, the right ventricular contraction and diastolic function decreased from 3 weeks after surgery (P < 0.01), and the right ventricle became hypertrophic from 4 weeks after (P < 0.05). Pressure-overload increased cardiomyocyte apoptosis from 4 weeks postoperatively (TUNEL staining and Western blotting analysis, P < 0.05); and fibrosis occurred in the right ventricular cardiomyocytes at 8 weeks after operation (Masson's trichrome stain, P < 0.01). In our model, pressure-overload to the right ventricle caused the right ventricular disorder, hypertrophy, and fibrosis. Apoptosis of right ventricular cardiomyocytes was involved in progression. We have shown for the first time the mechanism whereby pressure-overload right ventricular hypertrophy develops in an infant rabbit model.
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