Abstract
Pulmonary arterial hypertension (PAH) is a life-threatening disease that is characterized by an increase in pulmonary vascular pressure, leading to ventricular failure and high morbidity and mortality. Resveratrol, a phenolic compound and a sirtuin 1 pathway activator, has known dietary benefits and is used as a treatment for anti-inflammatory and cardiovascular diseases. Its therapeutic effects have been published in the scientific literature; however, its benefits in PAH are yet to be precisely elucidated. Using a murine model of PAH induced by monocrotaline, the macroscopic and microscopic effects of a daily oral dose of resveratrol in rats with PAH were evaluated by determining its impact on the lungs and the right and left ventricular function. While most literature has focused on smooth muscle cell mechanisms and lung pathology, our results highlight the relevance of therapy-mediated improvement of right ventricle and isolated cardiomyocyte physiology in both ventricles. Although significant differences in the pulmonary architecture were not identified either micro- or macroscopically, the effects of resveratrol on right ventricular function and remodeling were observed to be beneficial. The values for the volume, diameter, and contractility of the right ventricular cardiomyocytes returned to those of the control group, suggesting that resveratrol has a protective effect against ventricular dysfunction and pathological remodeling changes in PAH. The effect of resveratrol in the right ventricle delayed the progression of findings associated with right heart failure and had a limited positive effect on the architecture of the lungs. The use of resveratrol could be considered a future potential adjunct therapy, especially when the challenges to making a diagnosis and the current therapy limitations for PAH are taken into consideration.
Highlights
Pulmonary arterial hypertension (PAH) is a rare but progressive and often fatal pulmonary vascular disease [1]
Compared to the untreated control group (CTRL) (1.4 ± 0.2 g), heart weight increased by 21% in the PAH group (1:7 ± 0:2 g) and 35% with 1:7 ± 0:3 g for the PAH+RES group
Lungs weight followed the same trend: a weight increase of 2:0 ± 0:3 g was reported for the CTRL group, 45% increase was observed for the PAH group (2:9 ± 0:3 g), and a 60% increase was seen for the PAH+RES group (3:2 ± 0:4 g)
Summary
Pulmonary arterial hypertension (PAH) is a rare but progressive and often fatal pulmonary vascular disease [1]. PAH is characterized by a progressive increase in pulmonary vascular resistance and pulmonary arterial pressure, with secondary vascular and right ventricular (RV) remodeling, RV dysfunction, heart failure syndromes, and, premature death [2]. RES has been reported to have antifibrotic and anti-inflammatory effects in vivo [12] This compound has been evaluated in some PAH animal models for its ability to decrease lung damage in the tissue or pulmonary trunk [13], but the molecular mechanism of cardioprotection afforded by RES remains only partially understood. RES was demonstrated to be preferentially cardioprotective of the function and structure of the right ventricle, and it was shown to have a limited effect on the pulmonary vasculature
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