CRISTIANO TEIXEIRA MOSTARDA

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  • article 23 Citação(ões) na Scopus
    Baroreflex Sensitivity Impairment Is Associated With Cardiac Diastolic Dysfunction in Rats
    (2011) MOSTARDA, Cristiano; MORAES-SILVA, Ivana Cinthya; MOREIRA, Edson Dias; MEDEIROS, Alessandra; PIRATELLO, Aline Cristina; CONSOLIM-COLOMBO, Fernanda Marciano; CALDINI, Elia Garcia; BRUM, Patricia Chakur; KRIEGER, Eduardo Moacyr; IRIGOYEN, Maria Claudia
    Background: Studies have shown that the autonomic dysfunction accompanied by impaired baroreflex sensitivity was associated with higher mortality. However, the influence of decreased baroreflex sensitivity on cardiac function, especially in diastolic function, is not well understood. This study evaluated the morpho-functional changes associated with baroreflex impairment induced by chronic sinoaortic denervation (SAD). Methods and Results: Animals were divided into sinoaortic denervation (SAD) and control (C) groups. Baroreflex sensitivity was evaluated by tachycardic and bradycardic responses, induced by vasoactive drugs. Cardiac function was studied by echocardiography and by left ventricle (LV) catheterization. LV collagen content and the expression of regulatory proteins involved in intracellular Ca(2+) homeostasis were quantified. Results showed higher LV mass in SAD versus C animals. Furthermore, an increase in deceleration time of E-wave in the SAD versus the C group (2.14 +/- 0.07 ms vs 1.78 +/- 0.03 ms) was observed. LV end-diastolic pressure was increased and the minimum dP/dt was decreased in the SAD versus the C group (12 +/- 1.5 mm Hg vs 5.3 +/- 0.2 mm Hg and 7,422 +/- 201 vs 4,999 +/- 345 mm Hg/s, respectively). SERCA/NCX ratio was lower in SAD than in control rats. The same was verified in SERCA/PLB ratio. Conclusions: The results suggest that baroreflex dysfunction is associated with cardiac diastolic dysfunction independently of the presence of other risk factors. (J Cardiac Fail 2011;17:519-525)
  • article 9 Citação(ões) na Scopus
    Interval and continuous aerobic exercise training similarly increase cardiac function and autonomic modulation in infarcted mice
    (2017) ABAD, Cesar Cavinato Cal; NASCIMENTO, Ademir Manuel do; SANTOS, Leandro Eziquiel dos; FIGUEROA, Diego; RAMONA, Pamella; SARTORI, Michele; SCAPINI, Katie B.; ALBUQUERQUE, Oscar; MORAES-SILVA, Ivana Cinthya; COELHO-JUNIOR, Hello Jose; RODRIGUES, Bruno; MOSTARDA, Cristiano Teixeira; ANGELIS, Katia De; IRIGOYEN, Maria Claudia
    The present study aimed to compare the effects of moderate-intensity continuous and high-intensity interval exercise training (ET) on exercise tolerance, cardiac morphometry and function, hemodynamic, and cardiac autonomic modulation in myocardial infarcted mice. Wild-type mice (WT) were divided into four groups: sedentary WT (S); WT myocardium infarction sedentary (IS); WT myocardium infarction underwent to moderate-intensity continuous ET (MICT), and WT myocardium infarction underwent to high-intensity interval ET (MIIT). After 60 days of descending coronary artery ligation, moderate-intensity continuous ET consisted of running at 60% of maximum, while the high-intensity interval training consisted of eight sprints of 4 min at 80% of maximum and a 4-min recovery at 40% of maximum. Both exercises were performed 1 hr a day, 5 days a week, during 8 weeks. Results demonstrated that IS showed elevated exercise tolerance, as well as decreased hemodynamic and heart function, and autonomic control. On the other hand, both programs of ET were equally effective to increase all parameters, without further differences between the groups. In conclusion, the results of the present study showed that myocardial infarction leads to damage in both investigated strains and the two types of physical exercise attenuated the major impairments provoked by myocardial infarction in exercise tolerance, cardiac structure, cardiac function, hemodynamic and cardiac autonomic modulation.
  • article 16 Citação(ões) na Scopus
    Cardiac and pulmonary arterial remodeling after sinoaortic denervation in normotensive rats
    (2012) FLUES, K.; MORAES-SILVA, I. C.; MOSTARDA, C.; SOUZA, P. R. M.; DINIZ, G. P.; MOREIRA, E. D.; PIRATELLO, A. C.; CHAVES, M. L. Barreto; ANGELIS, K. De; SALEMI, Vera Maria Cury; IRIGOYEN, M. C.; CALDINI, E. G.
    Blood pressure variability (BPV) and baroreflex dysfunction may contribute to end-organ damage process. We investigated the effects of baroreceptor deficit (10 weeks after sinoaortic denervation - SAD) on hemodynamic alterations, cardiac and pulmonary remodeling. Cardiac function and morphology of male Wistar intact rats (C) and SAD rats (SAD) (n = 8/group) were assessed by echocardiography and collagen quantification. BP was directly recorded. Ventricular hypertrophy was quantified by the ratio of left ventricular weight (LVW) and right ventricular weight (RVW) to body weight (BW). BPV was quantified in the time and frequency domains. The atrial natriuretic peptide (ANP), alpha-skeletal actin (alpha-skelectal), collagen type I and type III genes mRNA expression were evaluated by RT-PCR. SAD did not change BP, but increased BPV (11 +/- 0.49 vs. 5 +/- 0.3 mm Hg). As expected, baroreflex was reduced in SAD. Pulmonary artery acceleration time was reduced in SAD. In addition, SAD impaired diastolic function in both LV (6.8 +/- 0.26 vs. 5.02 +/- 0.21 mm Hg) and RV (5.1 +/- 0.21 vs. 4.2 +/- 0.12 mm Hg). SAD increased LVW/BW in 9% and RVW/BW in 20%, and augmented total collagen (3.8-fold in LV, 2.7-fold in RV, and 3.35-fold in pulmonary artery). Also, SAD increased type I (similar to 6-fold) and III (similar to 5-fold) collagen gene expression. Denervation increased ANP expression in LV (75%), in RV (74%) and increased a-skelectal expression in LV (300%) and in RV (546%). Baroreflex function impairment by SAD, despite not changing BP, induced important adjustments in cardiac structure and pulmonary hypertension. These changes may indicate that isolated baroreflex dysfunction can modulate target tissue damage.
  • article 0 Citação(ões) na Scopus
    Interval and continuous aerobic exercise training similarly increase cardiac function and autonomic modulation in infarcted mice (vol 13, pg 257, 2017)
    (2017) ABAD, Cesar Cavinato Cal; NASCIMENTO, Ademir Manuel do; SOUZA, Leandro Eziquiel de; FIGUEROA, Diego; RAMONA, Pamella; SARTORI, Michele; SCAPINI, Katia B.; ALBUQUERQUE, Oscar; MORAES-SILVA, Ivana Cinthya; COELHO-JUNIOR, Helio Jose; RODRIGUES, Bruno; MOSTARDA, Cristiano Teixeira; ANGELIS, Katia De; IRIGOYEN, Maria Claudia
  • article 27 Citação(ões) na Scopus
    Exercise training prevents diastolic dysfunction induced by metabolic syndrome in rats
    (2012) MOSTARDA, Cristiano; MORAES-SILVA, Ivana Cinthya; SALEMI, Vera Maria Cury; MACHI, Jacqueline Freire; RODRIGUES, Bruno; ANGELIS, Katia De; FARAH, Vera de Moura Azevedo; IRIGOYEN, Maria Claudia
    OBJECTIVE: High fructose consumption contributes to the incidence of metabolic syndrome and, consequently, to cardiovascular outcomes. We investigated whether exercise training prevents high fructose diet-induced metabolic and cardiac morphofunctional alterations. METHODS: Wistar rats receiving fructose overload (F) in drinking water (100 g/l) were concomitantly trained on a treadmill (FT) for 10 weeks or kept sedentary. These rats were compared with a control group (C). Obesity was evaluated by the Lee index, and glycemia and insulin tolerance tests constituted the metabolic evaluation. Blood pressure was measured directly (Windaq, 2 kHz), and echocardiography was performed to determine left ventricular morphology and function. Statistical significance was determined by one-way ANOVA, with significance set at p<0.05. RESULTS: Fructose overload induced a metabolic syndrome state, as confirmed by insulin resistance (F: 3.6 +/- 0.2 vs. C: 4.5 +/- 0.2 mg/dl/min), hypertension (mean blood pressure, F: 118 +/- 3 vs. C: 104 +/- 4 mmHg) and obesity (F: 0.31 +/- 0.001 vs. C: 0.29 +/- 0.001 g/mm). Interestingly, fructose overload rats also exhibited diastolic dysfunction. Exercise training performed during the period of high fructose intake eliminated all of these derangements. The improvements in metabolic parameters were correlated with the maintenance of diastolic function. CONCLUSION: The role of exercise training in the prevention of metabolic and hemodynamic parameter alterations is of great importance in decreasing the cardiac morbidity and mortality related to metabolic syndrome.