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Induction of Right Ventricular Failure by Pulmonary Artery Constriction and Evaluation of Right Ventricular Function in Mice
Published on: May 13, 2019
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Maintained right ventricular pressure overload induces ventricular-arterial decoupling in mice.
Mario Boehm1, Allan Lawrie2, Jochen Wilhelm1
1Universities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardio-Pulmonary System (ECCPS), Member of the German Center for Lung Research (DZL), Giessen, Germany.
Experimental Physiology
|December 20, 2016
Summary
Combining echocardiography and pressure-volume catheterization effectively assesses right ventricular (RV) function in mice with pressure overload. This approach reveals ventricular-arterial decoupling and improves RV dysfunction phenotyping.
Area of Science:
- Cardiovascular Physiology
- Animal Models
- Echocardiography
- Hemodynamics
Background:
- Assessing right ventricular (RV) function in rodents is challenging due to complex anatomy.
- Current best practices combine non-invasive imaging and intracardiac pressure-volume measurements.
- A need exists for validated complementary techniques to evaluate RV function under pressure overload.
Purpose of the Study:
- To investigate the applicability of complementary non-invasive ultrasound imaging and closed-chest pressure-volume catheterization in mice.
- To enable in-depth characterization of right ventricular (RV) function during maintained pressure overload.
- To better phenotype RV function and dysfunction in genetically modified or pharmacologically treated mice.
Main Methods:
- Experimental mouse model of isolated RV pressure overload induced by pulmonary artery banding (n=8) or sham surgery (n=5).
- Assessment of RV function after 3 weeks using echocardiography (Vevo2100) and invasive pressure-volume measurements (PVR-1030).
- Analysis of RV hypertrophy, dilatation, systolic and diastolic dysfunction, and ventricular-arterial coupling.
Main Results:
- Pulmonary artery banding induced RV hypertrophy, dilatation, systolic, and diastolic dysfunction.
- Invasive hemodynamics showed increased RV end-systolic and arterial elastance, indicating ventricular-arterial decoupling.
- Tricuspid annular plane systolic excursion correlated with ventricular-arterial coupling, not RV contractility.
- Diastolic indices correlated well with RV end-diastolic pressure, demonstrating the combined approach's utility.
Conclusions:
- Complementary echocardiography and pressure-volume catheterization are feasible for detailed RV function assessment in mice.
- Systolic RV function indices reflect RV-arterial coupling, while diastolic indices correlate with RV end-diastolic pressure under overload.
- This combined approach enhances the phenotyping of RV function and dysfunction in preclinical research models.
