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Cited by 163Pulmonary Hypertension Research and TreatmentsCardiovascular Function and Risk FactorsCardiac Fibrosis and Remodeling

Characterization of right ventricular function after monocrotaline-induced pulmonary hypertension in the intact rat

Hessel, Marleen H. M., Steendijk, Paul, den Adel, Brigit, Schutte, Cindy I., van der Laarse, Arnoud·2006·American Journal of Physiology-Heart and Circulatory Physiology
DOI 10.1152/ajpheart.00369.2006
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Abstract

We characterized hemodynamics and systolic and diastolic right ventricular (RV) function in relation to structural changes in the rat model of monocrotaline (MCT)-induced pulmonary hypertension. Rats were treated with MCT at 30 mg/kg body wt (MCT30, n = 15) and 80 mg/kg body wt (MCT80, n = 16) to induce compensated RV hypertrophy and RV failure, respectively. Saline-treated rats served as control (Cont, n = 13). After 4 wk, a pressure-conductance catheter was introduced into the RV to assess pressure-volume relations. Subsequently, rats were killed, hearts and lungs were rapidly dissected, and RV, left ventricle (LV), and interventricular septum (IVS) were weighed and analyzed histochemically. RV-to-(LV + IVS) weight ratio was 0.29 ± 0.05 in Cont, 0.35 ± 0.05 in MCT30, and 0.49 ± 0.10 in MCT80 ( P < 0.001 vs. Cont and MCT30) rats, confirming MCT-induced RV hypertrophy. RV ejection fraction was 49 ± 6% in Cont, 40 ± 12% in MCT30 ( P < 0.05 vs. Cont), and 26 ± 6% in MCT80 ( P < 0.05 vs. Cont and MCT30) rats. In MCT30 rats, cardiac output was maintained, but RV volumes and filling pressures were significantly increased compared with Cont (all P < 0.05), indicating RV remodeling. In MCT80 rats, RV systolic pressure, volumes, and peak wall stress were further increased, and cardiac output was significantly decreased (all P < 0.05). However, RV end-systolic and end-diastolic stiffness were unchanged, consistent with the absence of interstitial fibrosis. MCT-induced pressure overload was associated with a dose-dependent development of RV hypertrophy. The most pronounced response to MCT was an overload-dependent increase of RV end-systolic and end-diastolic volumes, even under nonfailing conditions.

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Authors
Hessel, M. H. M., Steendijk, P., den Adel, B., Schutte, C. I., & van der Laarse, A.
Affiliations
Leiden University (NL)
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Publisher
American Physiological Society
Published
2006-11
Volume
291
Issue
5
Pages
H2424-H2430
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
DOI
10.1152/ajpheart.00369.2006
OpenAlex
W2169580681
Cited by
163
References
51
Citations by year
2026: 1 · 2025: 4 · 2024: 7 · 2023: 2 · 2022: 6 · 2021: 9 · 2020: 12 · 2019: 7 · 2018: 14 · 2017: 8 · 2016: 6 · 2015: 11 · 2014: 12 · 2013: 12 · 2012: 13
FWCI
5.57
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords
right ventricular function, monocrotaline, pulmonary hypertension, right ventricular hypertrophy, right heart failure, right ventricular remodeling, pressure-volume relationship, ejection fraction, wall stress, cardiac output, interstitial fibrosis, pressure overload, rat model
MeSH terms
Animals, Blood Pressure, Cardiac Output, Hypertension, Pulmonary, Immunohistochemistry, Male, Organ Size, Stroke Volume, Time Factors, Monocrotaline, Rats, Wistar, Hypertrophy, Right Ventricular, Ventricular Pressure, Ventricular Dysfunction, Right, Rats

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