RESUMEN
BACKGROUND: Pulmonary Arterial Hypertension (PAH) is a severe and progressive disease of pulmonary arterioles. This pathology is characterized by elevation of the pulmonary vascular resistance and pulmonary arterial pressure, leading to right heart failure and death. Studies have demonstrated that resveratrol possesses a protective effect on the mechanisms related to the genesis of the PAH-induced by different models. OBJECTIVE: This study aimed to investigate the dose-related effects of resveratrol in different models of pulmonary arterial hypertension. METHODS: To identify eligible papers, we performed a systematic literature search on Scielo, Pub- Med, and Scholar Google. The research was limited to articles written in English in the last 10 years. We used the following descriptors to search: Pulmonary Arterial Hypertension and Resveratrol, OR Resveratrol, and Animal models of Pulmonary Arterial Hypertension, OR Resveratrol, and in vitro models of Pulmonary Arterial Hypertension. RESULTS: 1724 studies were identified through the descriptors used, fifty-five studies with different models of pulmonary arterial hypertension were selected for the full review, forty-four were excluded after application of exclusion and inclusion criteria, totalizing eleven studies included in this systematic review. CONCLUSION: The results showed that resveratrol, at low and high doses, protects in a dosedependent manner against the development of PAH induced through monocrotaline, normoxia and hypoxia models. In addition to having chemopreventive, anti-inflammatory, antioxidant and antiproliferative properties. In the case of PAH-related myocardial injury, resveratrol protects cells from apoptosis, thus working as an antiapoptotic agent.
Asunto(s)
Antioxidantes/uso terapéutico , Hipertensión Arterial Pulmonar/tratamiento farmacológico , Resveratrol/uso terapéutico , Animales , Antioxidantes/farmacología , Modelos Animales de Enfermedad , Humanos , Masculino , Ratones , Resveratrol/farmacologíaRESUMEN
We tested whether hypertension favors the development of additional cardiometabolic changes in fructose-fed ovariectomized rats and how it affects aerobic exercise training (ET) effects. All rats received fructose in drinking water (10%) beginning at weaning, were ovariectomized at 10 weeks of age and divided into the normotensive sedentary (NFOS) and trained (NFOT) and hypertensive sedentary (HFOS) and trained (HFOT) groups. ET was performed on a treadmill. Arterial pressure (AP) was directly recorded; heart rate and AP variabilities were analyzed. Lipoperoxidation (LPO) and antioxidant enzyme levels were measured in the left ventricle. In addition to increased AP levels, when compared with the NFOS group, the hypertensive groups had resting tachycardia, a reduction of 29% in the pulse interval variance (VAR-PI), 19% in RMSSD (root mean square of successive differences, a cardiac parasympathetic index) and 53% in the α-index (spontaneous baroreflex), while the systolic AP variance (VAR-SAP) and its low-frequency band (LF-SAP) were sharply increased. ET did not alter AP levels. Even in the presence of hypertension, ET induced resting bradycardia, decreases of 33% in VAR-SAP and 49% in LF-SAP, and an increase of more than 60% in VAR-PI and the α-index. However, some of these parameters were still impaired relative to those of normotensive rats. LPO was reduced and catalase was increased in both trained groups, with no difference between the normotensive and hypertensive groups. Negative correlations were obtained between LPO and RMSSD (r=-0.60, P<0.05) and α-index (r=-0.63, P<0.05). In conclusion, hypertension augmented the dysfunctions in fructose-fed ovariectomized rats and attenuated metabolic aerobic ET benefits. These changes may be related to cardiovascular autonomic and oxidative stress alterations.