Fig. 1

Evaluation of pulmonary arterial hypertension by measuring mean pulmonary arterial pressure, right cardiac remodeling and function, and pulmonary arteries secretion of inflammatory cytokines. a Mean pulmonary arterial pressure (mPAP in mmHg) measured in controls rats (CTRL), after 4 weeks of chronic hypoxia (Hx), after 4 weeks of monocrotaline injection (MCT) or after combination of MCT and 3 or 4 weeks of Hx (3wk or 4wk MCT + Hx). Data represent means ± SEM with n = 13–14 rats per group. ***p < 0.001 versus controls. b Right ventricular hypertrophy expressed as the Fulton index (= Ratio of right ventricle weight (RV) to left ventricle plus septum weight (LV + S)) in the same experimental groups. Data represent means ± SEM with n = 14–15 rats per group. ***p < 0.001 versus controls and ^## p < 0.01 versus Hx. c Right heart ejection fraction (EF%) in CTRL or after combination of MCT and 3 or 4 weeks of Hx. Data represent means ± SEM with n = 6–8 rats per group. **p < 0.01 versus controls. d-e Secretion of the pro-inflammatory cytokines interleukin-1β (IL-1β, d) and tumor necrosis factor-α (TNF-α, e) by pulmonary arteries in control rats (CTRL), after chronic hypoxia (Hx), after monocrotaline treatment (MCT), or in rats treated with MCT and exposed to 4 weeks of Hx (4 wk MCT + Hx). Cytokines were determined by ELISA (results expressed as pg cytokine/ml supernatant after 24 h of incubation in the culture medium and presented as a percentage of cytokine secretion compared to controls). Data represent means ± SEM with n = 6 rats per group. **p < 0.01 and ***p < 0.001 versus controls. For all experiments, determination of statistically significant differences was assessed with a one-way analysis of variance followed by a Dunn test