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Characterization of a rat model of right-sided heart failure induced by pulmonary trunk banding
Authors:Uffe K Schou  Christian D Peters  Soo Wan Kim  Jrgen Frkir  Sren Nielsen
Institution:

aThe Water and Salt Research Center, Department of Anatomy, Building 233/234, University of Aarhus, DK-8000 Aarhus C, Denmark

bDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea

cClinical Institute, University of Aarhus, Brendstrupgaardsvej 100, Aarhus, Denmark

Abstract:Animal models of disease are essential for cardiovascular research. However, animal models of right-sided heart failure are few and remain poorly characterized. The aim with this study was to establish a rat model of right-sided heart failure (HF) using pulmonary trunk banding (PTB) and subsequently to characterize the systemic and cardiac changes in this model, including protein expression of SERCA2 and greek small letter alpha-sarcomeric actin. Rats underwent banding or sham operation. To evaluate the development of HF over time three groups were included in this study. They were killed 2–3, 5–7 or 16–17 weeks after operation, respectively. PTB rats showed marked hypertrophy of the right ventricle (RV). Catheterization of the RV showed a three- to four-fold increase in right ventricular systolic and diastolic pressures as well as increased dP/dT max and dP/dT min. Plasma analyses revealed increased liver enzymes in most PTB groups and post mortem examination revealed congestion of the liver as well as formation of ascites and hydrothorax in many PTB rats. Immunoblotting of the RV revealed no changes in SERCA2 or greek small letter alpha-sarcomeric actin. In conclusion, PTB was an effective method to induce right-sided HF. The presence of HF was confirmed by severe signs of backward failure in conjunction with markedly elevated RV pressures and reduced RV ejection fraction (EF).
Keywords:Right-sided heart failure  Hypertrophy  Animal models  Pulmonary hypertension  Echocardiography  Pulmonary trunk banding  Actin  SERCA2
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