The outcome of patients suffering from pulmonary arterial hypertension (PAH) are predominantly determined by the response of the right ventricle to the increase afterload secondary to high vascular pulmonary resistance. However, little is known about the effects of the current available or experimental PAH treatments on the heart.
Recently, inflammation has been implicated in the pathophysiology of PAH. N-acetylcysteine (NAC), a well-known safe anti-oxidant drug, has immuno-modulatory and cardioprotective properties.
We therefore hypothesized that NAC could reduce the severity of pulmonary hypertension (PH) in rats exposed to monocrotaline (MCT), lowering inflammation and preserving pulmonary vascular system and right heart function.
Methods:
Saline-treated control, MCT-exposed, MCT-exposed and NAC treated rats (day 14-28) were evaluated at day 28 following MCT for hemodynamic parameters (right ventricular systolic pressure, mean pulmonary arterial pressure and cardiac output), right ventricular hypertrophy, pulmonary vascular morphometry, lung inflammatory cells immunohistochemistry (monocyte/macrophages and dendritic cells), IL-6 expression, cardiomyocyte hypertrophy and cardiac fibrosis.
Results:
The treatment with NAC significantly decreased pulmonary vascular remodeling, lung inflammation, and improved total pulmonary resistance (from 0.71 +/- 0.05 for MCT group to 0.50 +/- 0.06 for MCT + NAC group, p
439 +/- 21 mum2 for MCT and MCT + NAC group respectively, p
Conclusions:
Through its immuno-modulatory and cardioprotective properties, NAC has beneficial effect on pulmonary vascular and right heart function in experimental PH.
Author: Marie-Camille ChaumaisBenoit RanchouxDavid MontaniPeter DorfmüllerLy TuFlorence LecerfNicolas RaymondChristophe GuignabertLaura PriceGérald SimonneauSylvia Cohen-KaminskyMarc HumbertFrédéric Perros
Credits/Source: Respiratory Research 2014,
Published on: 2014-06-14
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