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Updated: Feb 26, 2026
A Pulmonary Trunk Banding Model of Pressure Overload Induced Right Ventricular Hypertrophy and Failure
Published on: November 29, 2018
A neonatal rat model of increased right ventricular afterload by pulmonary artery banding
Shoubao Wang1, Lincai Ye2, Haifa Hong1
1Department of Thoracic and Cardiovascular Surgery, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.
Objective:
To construct a neonatal rat model of increased right ventricular (RV) afterload for studying the pathophysiological remodeling of the right ventricle in patients with congenital heart disease with increased RV afterload.
Methods:
Surgery was performed within 6 hours after birth. Horizontal thoracotomy was performed by dissecting the intercostal muscles and splitting the sternum. The PA was then banded with 11-0 nylon thread. At postnatal day 7 (P7), constriction of PA was confirmed by echocardiography. The RV systolic and diastolic pressures were measured by cardiac catheterization. The RV end-systolic volume, end-diastolic volume, end-diastolic diameter, and free wall thickness were assessed by magnetic resonance imaging. The histological changes in sham-operated and PA-banding (PAB) hearts were evaluated by hematoxylin and eosin staining.
Results:
Increased RV afterload was established by constriction of the PA in neonatal rats within 6 hours after birth. The survival rate was 75% at P7. Relative to the sham group, the peak pressure gradient across the PA constriction and RV systolic and diastolic pressures, end-systolic volume, end-diastolic volume, end-diastolic diameter, and free wall thickness were significantly increased in the PAB group at P7 (P < .01). Consistently, histological examination showed that the RV free wall was significantly hypertrophic in the PAB group.
Conclusions:
We successfully established a neonatal RV afterload increase model through PAB within 6 hours after birth, which can be used to study the pathophysiological changes in congenital heart diseases with increased RV afterload.
