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Updated: Aug 8, 2026
Comprehensive Echocardiographic Assessment of Right Ventricle Function in a Rat Model of Pulmonary Arterial Hypertension
Published on: January 20, 2023
Characterization of right ventricular function after monocrotaline-induced pulmonary hypertension in the intact rat
Marleen H M Hessel1, Paul Steendijk, Brigit den Adel
1Dept. of Cardiology, C5-P, Leiden Univ. Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands.
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.
Insights
Monocrotaline (MCT) induced dose-dependent right ventricular (RV) hypertrophy and remodeling in rats. Even without failure, RV volumes increased, showing significant changes in RV function under pressure overload.
Area of Science:
- Cardiovascular Physiology
- Pulmonary Hypertension Research
- Animal Models in Cardiology
Background:
- Pulmonary hypertension (PH) leads to right ventricular (RV) dysfunction and failure.
- Understanding RV structural and functional changes in response to pressure overload is crucial for developing effective treatments.
- The monocrotaline (MCT) rat model is widely used to study PH and its effects on the RV.
Purpose of the Study:
- To characterize hemodynamics and RV function in relation to structural changes in a rat model of MCT-induced pulmonary hypertension.
- To investigate the dose-dependent effects of MCT on RV hypertrophy, remodeling, and function.
- To assess RV systolic and diastolic function and stiffness in compensated and failing RV states.
Main Methods:
- Rats were treated with varying doses of monocrotaline (MCT) to induce pulmonary hypertension.
- Hemodynamic parameters and RV pressure-volume relations were assessed using a pressure-conductance catheter.
- RV, left ventricle (LV), and interventricular septum (IVS) weights were measured, and histochemical analysis was performed.
Main Results:
- MCT treatment resulted in a dose-dependent increase in RV hypertrophy, confirmed by increased RV/(LV + IVS) weight ratio.
- RV ejection fraction was significantly reduced in MCT-treated rats, indicating impaired systolic function.
- MCT30 rats showed maintained cardiac output but increased RV volumes and filling pressures (remodeling), while MCT80 rats exhibited decreased cardiac output and increased RV pressures and volumes.
Conclusions:
- MCT-induced pressure overload causes dose-dependent RV hypertrophy and remodeling.
- Increased RV end-systolic and end-diastolic volumes occur even in compensated RV states, highlighting early adaptive changes.
- RV stiffness remained unchanged, suggesting interstitial fibrosis was not a primary factor in this model.
