CRISTIANO TEIXEIRA MOSTARDA

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  • article 22 Citação(ões) na Scopus
    Metabolic, hemodynamic and structural adjustments to low intensity exercise training in a metabolic syndrome model
    (2013) MORVAN, Eduardo; LIMA, Nathalia Edviges Alves; MACHI, Jacqueline Freire; MOSTARDA, Cristiano; ANGELIS, Katia De; IRIGOYEN, Maria Claudia; WICHI, Rogerio Brandao; RODRIGUES, Bruno; MAIFRINO, Laura Beatriz Mesiano
    Background: The increase in fructose consumption is paralleled by a higher incidence of metabolic syndrome, and consequently, cardiovascular disease mortality. We examined the effects of 8 weeks of low intensity exercise training (LET) on metabolic, hemodynamic, ventricular and vascular morphological changes induced by fructose drinking in male rats. Methods: Male Wistar rats were divided into (n = 8 each) control (C), sedentary fructose (F) and ET fructose (FT) groups. Fructose-drinking rats received D-fructose (100 g/l). FT rats were assigned to a treadmill training protocol at low intensity (30% of maximal running speed) during 1 h/day, 5 days/week for 8 weeks. Measurements of triglyceride concentrations, white adipose tissue (WAT) and glycemia were carried out together with insulin tolerance test to evaluate metabolic profile. Arterial pressure (AP) signals were directly recorded. Baroreflex sensitivity (BS) was evaluated by the tachycardic and bradycardic responses. Right atria, left ventricle (LV) and ascending aorta were prepared to morphoquantitative analysis. Results: LET reduced WAT (-37.7%), triglyceride levels (-33%), systolic AP (-6%), heart weight/body weight (-20.5%), LV (-36%) and aortic (-76%) collagen fibers, aortic intima-media thickness and circumferential wall tension in FT when compared to F rats. Additionally, FT group presented improve of BS, numerical density of atrial natriuretic peptide granules (+42%) and LV capillaries (+25%), as well as the number of elastic lamellae in aorta compared with F group. Conclusions: Our data suggest that LET, a widely recommended practice, seems to be particularly effective for preventing metabolic, hemodynamic and morphological disorders triggered by MS.
  • article 21 Citação(ões) na Scopus
    Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats
    (2014) MALFITANO, Christiane; BARBOZA, Catarina Andrade; MOSTARDA, Cristiano; PALMA, Renata Kelly da; SANTOS, Camila Paixao dos; RODRIGUES, Bruno; FREITAS, Sarah Cristina Ferreira; BELLO-KLEIN, Adriane; LLESUY, Susana; IRIGOYEN, Maria-Claudia; ANGELIS, Katia De
    Background: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. The aim of the present study was to investigate the association between hyperglycemia and myocardial infarction on cardiovascular autonomic modulation and cardiac oxidative stress profile in rats. Male Wistar rats were divided into: control (C), diabetic (D), myocardial infarcted (MI) and diabetic infarcted rats (DMI). Methods: Diabetes was induced by streptozotocin (STZ, 50 mg/Kg) at the beginning of the protocol and MI was induced by left coronary occlusion 15 days after STZ. Thirty days after streptozocin-induced diabetes, cardiovascular autonomic modulation was evaluated by spectral analysis, and oxidative stress profile was determined by antioxidant enzyme activities and superoxide anion, together with protein carbonylation and redox balance of glutathione (GSH/GSSG). Results: The diabetic and infarcted groups showed decreased heart rate variability and vagal modulation (p < 0.05); however, sympathetic modulation decreased only in diabetic groups (p < 0.05). Sympatho/vagal balance and vascular sympathetic modulation were increased only in the MI group (p < 0.05). Diabetes promoted an increase in catalase concentration (p < 0.05). Glutathione peroxidase activity was increased only in DMI when compared to the other groups (p < 0.05). Superoxide anion and protein carbonylation were increased only in MI group (p < 0.05). Cardiac redox balance, as evaluated by GSH/GSSG, was lower in the MI group (p < 0.05). Conclusions: These data suggest that hyperglycemia promotes compensatory mechanisms that may offer protection against ischemia, as demonstrated by increased antioxidants, decreased pro-oxidants and protein damage, possibly related to the improvements in both redox balance and sympathetic modulation to the heart.