Fig. 1From: Chronic hypoxia aggravates monocrotaline-induced pulmonary arterial hypertension: a rodent relevant model to the human severe form of the diseaseEvaluation 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 testBack to article page