ArticlePulmonary circulation
Compensated right ventricular function of the onset of pulmonary hypertension in a rat model depends on chamber remodeling and contractile augmentation.
Article in Pulmonary circulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Skeletal muscle histological remodeling precedes functional impairment in a muscle-specific manner following monocrotaline-induced heart failure in rats.European journal of applied physiology · 2026Article
- Sex and ovarian hormone status shape baseline cardiovascular physiology in Sprague Dawley rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Article
- Ovarian hormones attenuate right ventricular remodeling in a rat model of pulmonary arterial hypertension.Biomechanics and modeling in mechanobiology · 2025Article
- Sexually dimorphic role of estrogen receptor α in preserving right ventricular endothelial integrity.bioRxiv : the preprint server for biology · 2025Article
- Cardiac function at follow-up in infants treated with therapeutic hypothermia for neonatal hypoxic-ischemic encephalopathy.Pediatric research · 2025Article
- NLRP3 inflammasome activation by turbulent shear stress drives right ventricular outflow tract fibrosis in pulmonary regurgitation.Frontiers in cardiovascular medicine · 2025Article
- Magnetic nanoradiotracers for targeted neutrophil detection in pulmonary arterial hypertension.Journal of nanobiotechnology · 2024Article
- Sex-dependent remodeling of right ventricular function in a rat model of pulmonary arterial hypertension.American journal of physiology. Heart and circulatory physiology · 2024Article
- A perfectly imperfect engine: Utilizing the digital twin paradigm in pulmonary hypertension.Pulmonary circulation · 2024Review
- A computational study of right ventricular mechanics in a rat model of pulmonary arterial hypertension.Frontiers in physiology · 2024Article
- Untangling the mechanisms of pulmonary arterial hypertension-induced right ventricular stiffening in a large animal model.Acta biomaterialia · 2023Article
- Untangling the mechanisms of pulmonary hypertension-induced right ventricular stiffening in a large animal model.bioRxiv : the preprint server for biology · 2023Article
- Right Ventricular Architectural Remodeling and Functional Adaptation in Pulmonary Hypertension.Circulation. Heart failure · 2023Article
- Effects of the peripheral CBFrontiers in pharmacology · 2022Article
- Computational models of ventricular mechanics and adaptation in response to right-ventricular pressure overload.Frontiers in physiology · 2022Review
- Distinct time courses and mechanics of right ventricular hypertrophy and diastolic stiffening in a male rat model of pulmonary arterial hypertension.American journal of physiology. Heart and circulatory physiology · 2021Article
- Current Understanding of the Right Ventricle Structure and Function in Pulmonary Arterial Hypertension.Frontiers in physiology · 2021Review
- Multiscale Modeling Framework of Ventricular-Arterial Bi-directional Interactions in the Cardiopulmonary Circulation.Frontiers in physiology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Right-ventricular function is a good indicator of pulmonary arterial hypertension (PAH) prognosis; however, how the right ventricle (RV) adapts to the pressure overload is not well understood. Here, we aimed at characterizing the time course of RV early remodeling and discriminate the contribution of ventricular geometric remodeling and intrinsic changes in myocardial mechanical properties in a monocrotaline (MCT) animal model. In a longitudinal study of PAH, ventricular morphology and function were assessed weekly during the first four weeks after MCT exposure. Using invasive measurements of RV pressure and volume, heart performance was evaluated at end of systole and diastole to quantify contractility (end-systolic elastance) and chamber stiffness (end-diastolic elastance). To distinguish between morphological and intrinsic mechanisms, a computational model of the RV was developed and used to determine the level of prediction when accounting for wall masses and unloaded volume measurements changes. By four weeks, mean pulmonary arterial pressure and elastance rose significantly. RV pressures rose significantly after the second week accompanied by significant RV hypertrophy, but RV stroke volume and cardiac output were maintained. The model analysis suggested that, after two weeks, this compensation was only possible due to a significant increase in the intrinsic inotropy of RV myocardium. We conclude that this MCT-PAH rat is a model of RV compensation during the first month after treatment, where geometric remodeling on EDPVR and increased myocardial contractility on ESPVR are the major mechanisms by which stroke volume is preserved in the setting of elevated pulmonary arterial pressure. The mediators of this compensation might themselves promote longer-term adverse remodeling and decompensation in this animal model.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.