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Exercise training modulates right ventricular function and remodeling in experimental pulmonary arterial hypertension
Author(s) -
Gonçalves Daniel,
Fonseca Hélder,
Ferreira Rita,
Padrão Ana Isabel,
Vasques-Nóvoa Francisco,
Vieira Sara,
Pinto Manuel,
Gonçalves Nadia,
Neto Marina,
Paixão Rodney,
Amado Francisco,
Duarte José Alberto,
Leite-Moreira Adelino,
Henriques-Coelho Tiago
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.872.8
Subject(s) - pressure overload , ventricle , medicine , cardiology , pulmonary hypertension , cardiac function curve , heart failure , ventricular pressure , ventricular remodeling , muscle hypertrophy , right ventricular hypertrophy , blood pressure , cardiac hypertrophy
Right ventricle failure (RVF) is a major determinant of survival in pulmonary arterial hypertension (PAH). Exercise training was shown to be beneficial in left ventricle failure but its impact on RVF remains unknown. We investigated whether exercise training modulates the right ventricular response to chronic pressure overload in monocrotaline (MCT) model of PAH. Male Wistar rats were submitted to normal cage activity (SED+MCT) or to treadmill exercise training (EXtreat+MCT) after the establishment of RV pressure overload induced by MCT (60 mg/kg). Exercise training attenuated cardiac hypertrophy, improved cardiac function and survival. Exercise training normalized RV SERCA2a protein levels, beta/alpha MHC isoform, ET‐1 and VEGF mRNA, cardiac fibrosis and inflammation. Mitochondrial function was preserved and was accompanied by reduced oxidative damage. These data suggest that exercise training is cardioprotective in RVF induced by experimental PAH and provide some insights about the putative underlying cardioprotective mechanisms.