RT Journal Article
SR Electronic
T1 Dehydroepiandrosterone reverses chronic hypoxia/reoxygenation-induced right ventricular dysfunction in rats
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 1420
OP 1429
DO 10.1183/09031936.00011511
VO 40
IS 6
A1 Eric Dumas de La Roque
A1 Nadège Bellance
A1 Rodrigue Rossignol
A1 Hugues Begueret
A1 Marie Billaud
A1 Pierre Dos Santos
A1 Thomas Ducret
A1 Roger Marthan
A1 Diana Dahan
A1 David Ramos-Barbón
A1 Óscar Amor-Carro
A1 Jean-Pierre Savineau
A1 Michael Fayon
YR 2012
UL http://erj.ersjournals.com/content/40/6/1420.abstract
AB Dehydroepiandrosterone (DHEA) prevents chronic hypoxia-induced pulmonary hypertension and associated right ventricle dysfunction in rats. In this animal model, reoxygenation following hypoxia reverses pulmonary hypertension but not right ventricle dysfunction. We thus studied the effect of DHEA on the right ventricle after reoxygenation, i.e. after a normoxic recovery phase secondary to chronic hypoxia in rats. Right ventricle function was assessed in vivo by Doppler echocardiography and in vitro by the isolated perfused heart technique in three groups of animals: control, recovery (21 days of hypoxia followed by 21 days of normoxia) and recovery DHEA (30 mg·kg−1 every 2 days during the recovery phase). Right ventricle tissue was assessed by optical and electron microscopy. DHEA abolished right ventricle diastolic dysfunction, as the echographic E wave remained close to that of controls (mean±sd 76.5±2.4 and 79.7±1.7 cm·s−1, respectively), whereas it was diminished to 40.3±3.7 in the recovery group. DHEA also abolished right ventricle systolic dysfunction, as shown by the inhibition of the increase in the slope of the pressure–volume curve in isolated heart. The DHEA effect was related to cardiac myocytes proliferation. In conclusion, DHEA prevents right ventricle dysfunction in this animal model by preventing cardiomyocyte alteration.