Diego Figueroa

Instituto do Coração, San Paulo, São Paulo, Brazil

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Publications (10)22.25 Total impact

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    ABSTRACT: The aim of this study was to evaluate the effects of aerobic exercise training or resistance exercise training on cardiac morphometric, functional, and oxidative stress parameters in rats with ovarian hormone deprivation and diabetes.
    Menopause (New York, N.Y.) 10/2014; · 3.08 Impact Factor
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    ABSTRACT: It has been suggested that exercise training (ET) protects against the pathological remodeling and ventricular dysfunction induced by myocardial infarction (MI). However, it remains unclear whether the positive adjustments on baroreflex and cardiac autonomic modulations promoted by ET may afford a cardioprotective mechanism. The aim of this study was to evaluate the effects of aerobic ET, prior to MI, on cardiac remodeling and function, as well as on baroreflex sensitivity and autonomic modulation in rats.
    BMC Cardiovascular Disorders 07/2014; 14(1):84. · 1.46 Impact Factor
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    ABSTRACT: Background: Although resistance exercise training is part of cardiovascular rehabilitation programs, little is known about its role on the cardiac and autonomic function after myocardial infarction. Objective: To evaluate the effects of resistance exercise training, started early after myocardial infarction, on cardiac function, hemodynamic profile, and autonomic modulation in rats. Methods: Male Wistar rats were divided into four groups: sedentary control, trained control, sedentary infarcted and trained infarcted rats. Each group with n = 9 rats. The animals underwent maximum load test and echocardiography at the beginning and at the end of the resistance exercise training (in an adapted ladder, 40% to 60% of the maximum load test, 3 months, 5 days/week). At the end, hemodynamic, baroreflex sensitivity and autonomic modulation assessments were made. Results: The maximum load test increased in groups trained control (+32%) and trained infarcted (+46%) in relation to groups sedentary control and sedentary infarcted. Although no change occurred regarding the myocardial infarction size and systolic function, the E/A ratio (-23%), myocardial performance index (-39%) and systolic blood pressure (+6%) improved with resistance exercise training in group trained infarcted. Concomitantly, the training provided additional benefits in the high frequency bands of the pulse interval (+45%), as well as in the low frequency band of systolic blood pressure (-46%) in rats from group trained infarcted in relation to group sedentary infarcted. Conclusion: Resistance exercise training alone may be an important and safe tool in the management of patients after myocardial infarction, considering that it does not lead to significant changes in the ventricular function, reduces the global cardiac stress, and significantly improves the vascular and cardiac autonomic modulation in infarcted rats.
    Arquivos Brasileiros de Cardiologia 07/2014; · 1.13 Impact Factor
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    ABSTRACT: The aim of this study was to evaluate the effects of exercise training (ET, 50-70% of VO2 max, 5 days/week) and detraining (DT) on inflammatory and metabolic profile after myocardial infarction (MI) in rats. Male Wistar rats were divided into control (C, n = 8), sedentary infarcted (SI, n = 9), trained infarcted (TI, n = 10; 3 months of ET), and detrained infarcted (DI, n = 11; 2 months of ET + 1 month of DT). After ET and DT protocols, ventricular function and inflammation, cardiovascular autonomic modulation (spectral analysis), and adipose tissue inflammation and lipolytic pathway were evaluated. ET after MI improved cardiac and vascular autonomic modulation, and these benefits were correlated with reduced inflammatory cytokines on the heart and adipose tissue. These positive changes were sustained even after 1 month of detraining. No expressive changes were observed in oxidative stress and lipolytic pathway in experimental groups. In conclusion, our results strongly suggest that the autonomic improvement promoted by ET, and maintained even after the detraining period, was associated with reduced inflammatory profile in the left ventricle and adipose tissue of rats subjected to MI. These data encourage enhancing cardiovascular autonomic function as a therapeutic strategy for the treatment of inflammatory process triggered by MI.
    Mediators of Inflammation 01/2014; 2014:207131. · 3.88 Impact Factor
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    ABSTRACT: We evaluate the effects of detraining (DT, for 1 month) on the left ventricular (LV) remodeling and function, hemodynamic and baroreflex sensitivity (BRS), as well as on mortality rate of infarcted (MI) rats after 3 months of exercise training (ET, 50-70 % of VO(2max)). Male Wistar rats were divided into five groups: control (C, n = 10), untrained-infarcted (UI, n = 15), trained-infarcted (TI, n = 12), untrained-infarcted plus 1 month (UI-1, n = 15) and detrained-infarcted 1 month (DI-1, n = 15). LV function was evaluated by echocardiography at the initial and final of the protocols. After following, ET and/or DT protocols, hemodynamic and BRS [by tachycardic (TR) and bradycardic (BR) responses] were assessed. TI group displayed increased VO(2max) in comparison with UI and DI-1 groups; however, DI-1 values remained increased compared to UI-1 group. MI area was reduced by ET and maintained after DT. Ejection fraction (TI = 60 ± 2 and DI-1 = 61 ± 2 % vs. UI = 41 ± 1 and UI-1 = 37 ± 3 %), E/A ratio (TI = 1.6 ± 0.1 and DI-1 = 1.9 ± 0.1 vs. UI = 2.9 ± 0.2 and UI-1 = 2.9 ± 0.3), TR (TI = 3.3 ± 0.3 and DI-1 = 3.3 ± 0.4 vs. UI = 1.7 ± 0.1 and UI-1 = 1.6 ± 0.1 bpm/mmHg) and BR (TI = -2.2 ± 0.1 and DI-1 = -2.0 ± 0.1 vs. UI = -1.3 ± 0.09 and UI-1 = -1.2 ± 0.09 bpm/mmHg) were improved by ET and maintained after DT in comparison with untrained rats. These changes resulted in mortality reduction in the TI (8 %) and DI-1 groups (13 %) compared with the UI (46 %) and UI-1 (53 %) groups. These findings indicate that ET is not only an effective tool in the management of cardiovascular and autonomic MI derangements, but also that these positive changes were maintained even after 1 month of DT in rats.
    Arbeitsphysiologie 10/2012; · 2.66 Impact Factor
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    ABSTRACT: To investigate the effects of hyperglycemia on left ventricular dysfunction, morphometry, myocardial infarction area, hemodynamic parameters, oxidative stress profile, and mortality rate in rats that had undergone seven days of myocardial infarction. Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. Male Wistar rats were divided into four groups: control-sham, diabetes-sham, myocardial infarction, and diabetes + myocardial infarction. Myocardial infarction was induced 14 days after diabetes induction. Ventricular function and morphometry, as well as oxidative stress and hemodynamic parameters, were evaluated after seven days of myocardial infarction. The myocardial infarction area, which was similar in the infarcted groups at the initial evaluation, was reduced in the diabetes + myocardial infarction animals (23 ± 3%) when compared with the myocardial infarction (42 ± 7%, p < 0.001) animals at the final evaluation. The ejection fraction (22%, p = 0.003), velocity of circumferential fiber shortening (30%, p = 0.001), and left ventricular isovolumetric relaxation time (26%, p = 0.002) were increased in the diabetes + myocardial infarction group compared with the myocardial infarction group. The diabetes-sham and diabetes + myocardial infarction groups displayed increased catalase concentrations compared to the control-sham and myocardial infarction groups (diabetes-sham: 32 ± 3; diabetes + myocardial infarction: 35 ± 0.7; control-sham: 12 ± 2; myocardial infarction: 16 ± 0.1 pmol min⁻¹ mg⁻¹ protein). The levels of thiobarbituric acid-reactive substances were reduced in the diabetes-sham rats compared to the control-sham rats. These positive adaptations were reflected in a reduced mortality rate in the diabetes + myocardial infarction animals (18.5%) compared with the myocardial infarction animals (40.7%, p = 0.001). These data suggest that short-term hyperglycemia initiates compensatory mechanisms, as demonstrated by increased catalase levels, which culminate in improvements in the ventricular response, infarcted area, and mortality rate in diabetic rats exposed to ischemic injury.
    Clinics (São Paulo, Brazil) 01/2011; 66(8):1437-42. · 1.59 Impact Factor
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    ABSTRACT: Objective: The aim of this study was to investigate the effects of exercise training on cardiovascular autonomic dysfunction in ovariectomized rats submitted to myocardial infarction. Methods: Female Wistar rats were divided into the following ovariectomized groups: sedentary ovariectomized (SO), trained ovariectomized (TO), sedentary ovariectomized infarcted (SOI), and trained ovariectomized infarcted (TOI). Trained groups were submitted to an exercise training protocol on a treadmill (8 wk). Arterial baroreflex sensitivity was evaluated by heart rate responses to arterial pressure changes, and cardiopulmonary baroreflex sensitivity was tested by bradycardic and hypotension responses to serotonin injection. Vagal and sympathetic effects were calculated by pharmacological blockade. Results: Arterial pressure was reduced in the TO in comparison with the SO group and increased in the TOI in relation to the SOI group. Exercise training improved the baroreflex sensitivity in both the TO and TOI groups. The TOI group displayed improvement in cardiopulmonary reflex sensitivity compared with the SOI group at the 16 μg/kg serotonin dose. Exercise training enhanced the vagal effect in both the TO (45%) and TOI (46%) animals compared with the SO and SOI animals and reduced the sympathetic effect in the TOI (38%) in comparison with the SOI animals. Significant correlations were obtained between bradycardic baroreflex responses and vagal (r = −0.7, P < 0.005) and sympathetic (r = 0.7, P < 0.001) effects. Conclusions: These results indicate that exercise training in ovariectomized rats submitted to myocardial infarction improves resting hemodynamic status and reflex control of the circulation, which may be due to an increase in the vagal component. This suggests a homeostatic role for exercise training in reducing the autonomic impairment of myocardial infarction in postmenopausal women.
    Menopause 06/2010; 17(4):712-717. · 3.16 Impact Factor
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    ABSTRACT: The objective of the present study was to identify metabolic, cardiovascular and autonomic changes induced by fructose overload administered in the drinking water of rats for 8 weeks. Female Wistar rats (200-220 g) were divided into 2 groups: control (N = 8) and fructose-fed rats (N = 5; 100 mg/L fructose in drinking water for 8 weeks). The autonomic control of heart rate was evaluated by pharmacological blockade using atropine (3 mg/kg) and propranolol (4 mg/kg). The animals were submitted to an intravenous insulin tolerance test (ITT) and to blood glucose measurement. The fructose overload induced a significant increase in body weight (approximately 10%) and in fasting glycemia (approximately 28%). The rate constant of glucose disappearance (KITT) during ITT was lower in fructose-fed rats (3.25 +/- 0.7%/min) compared with controls (4.95 +/- 0.3%/min, P < 0.05) indicating insulin resistance. The fructose-fed group presented increased arterial pressure compared to controls (122 +/- 3 vs 108 +/- 1 mmHg, P < 0.05) and a reduction in vagal tonus (31 +/- 9 vs 55 +/- 5 bpm in controls, P < 0.05). No changes in sympathetic tonus were observed. A positive correlation, tested by the Pearson correlation, was demonstrable between cardiac vagal tonus and KITT (r = 0.8, P = 0.02). These data provided new information regarding the role of parasympathetic dysfunction associated with insulin resistance in the development of early metabolic and cardiovascular alterations induced by a high fructose diet.
    Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas / Sociedade Brasileira de Biofisica ... [et al.] 09/2008; 41(9):804-8. · 1.08 Impact Factor
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    ABSTRACT: Abstract Background The aim of the present study was to investigate the relationship between speed during maximum exercise test (ET) and oxygen consumption (VO<sub>2</sub>) in control and STZ-diabetic rats, in order to provide a useful method to determine exercise capacity and prescription in researches involving STZ-diabetic rats. Methods Male Wistar rats were divided into two groups: control (CG, n = 10) and diabetic (DG, n = 8). The animals were submitted to ET on treadmill with simultaneous gas analysis through open respirometry system. ET and VO<sub>2 </sub>were assessed 60 days after diabetes induction (STZ, 50 mg/Kg). Results VO<sub>2 </sub>maximum was reduced in STZ-diabetic rats (72.5 ± 1 mL/Kg/min<sup>-1</sup>) compared to CG rats (81.1 ± 1 mL/Kg/min<sup>-1</sup>). There were positive correlations between ET speed and VO<sub>2 </sub>(r = 0.87 for CG and r = 0.8 for DG), as well as between ET speed and VO<sub>2 </sub>reserve (r = 0.77 for CG and r = 0.7 for DG). Positive correlations were also obtained between measured VO<sub>2 </sub>and VO<sub>2 </sub>predicted values (r = 0.81 for CG and r = 0.75 for DG) by linear regression equations to CG (VO<sub>2 </sub>= 1.54 * ET speed + 52.34) and DG (VO<sub>2 </sub>= 1.16 * ET speed + 51.99). Moreover, we observed that 60% of ET speed corresponded to 72 and 75% of VO<sub>2 </sub>reserve for CG and DG, respectively. The maximum ET speed was also correlated with VO<sub>2 </sub>maximum for both groups (CG: r = 0.7 and DG: r = 0.7). Conclusion These results suggest that: a) VO<sub>2 </sub>and VO<sub>2 </sub>reserve can be estimated using linear regression equations obtained from correlations with ET speed for each studied group; b) exercise training can be prescribed based on ET in control and diabetic-STZ rats; c) physical capacity can be determined by ET. Therefore, ET, which involves a relatively simple methodology and low cost, can be used as an indicator of cardio-respiratory capacity in future studies that investigate the physiological effect of acute or chronic exercise in control and STZ-diabetic male rats.
    Cardiovascular Diabetology 01/2007; · 4.21 Impact Factor