LEANDRO EZIQUIEL DE SOUZA
Índice h a partir de 2011
7
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
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conferenceObject Impact of sympathectomy upon myocardium(2019) PESSOA, F. Fernanda; JORDAO, M. R.; FONSECA, K. C. B.; ZANONI, F.; SALEMI, V. M. C.; RIBEIRO, O. N.; SOUZA, L. E.; FERNANDES, F.; IRIGOYEN, M. C.; MOREIRA, L. F. P.; MADY, C.; RAMIRES, F. J. A.conferenceObject Baroreflex and cardiac dysfunctions evaluated by transesophageal echocardiography, baroreflex sensitivity, autonomic control and invasive measurements in rats submitted to sinoaortic denervation(2012) SIRVENTE, R. A.; IRIGOYEN, M. C.; SOUZA, L.; MOSTARDA, C.; FUENTE, R. La; CANDIDO, G.; SOUZA, P.; MEDEIROS, A.; MADY, C.; SALEMI, V. M. C.Purpose: Sympathetic hyperactivity commonly seems to be related to cardiac dysfunction and baro and chemoreflexes impairment in hypertension. However, myocardial function has not been evaluated regarding the association of hypertension and baroreflex dysfunction using transesophageal echocardiography. Methods: Exercise test (ET), baroreflex sensitivity, cardiovascular autonomic control, transthoracic and transesophageal echocardiography using intracardiac echocardiographic catheter (AcuNav, Siemens, Mountain View, CA, USA), and invasively biventricular end-diastolic pressures (EDP) were evaluated in rats 10 weeks after sinoaortic denervation (SAD). The rats (n=32) were divided in 4 groups: 16 Wistar (W) with (n=8) or without SAD (n=8) and 16 spontaneously hypertensive rats (SHR) with (n=8) or without SAD (n=8). Results: Blood pressure (BP) and heart rate (HR) did not show any change between the groups SAD and without SAD, although, SHR showed higher BP levels in comparison to W. BP variability was increased in SHR groups compared to W. After SAD, BP variability increased in all groups compared to W (W: 15 mmHg2; *DSA: 49 mmHg2; *SHR: 60 mmHg2; *SHR-SAD:137 mmHg2, *p<0.05 vs. W). Exercise tests results showed that SHR had better functional capacity compared to SAD and SHRSAD (W: 1.16m/s; DSA: 0.9m/s; *SHR: 1.46; SHR-DSA: 1.02, *p<0.05 vs. SAD and SHRSAD). Left ventricular concentric hypertrophy, segmental systolic dysfunction and global diastolic LV dysfunction, segmental and global systolic dysfunction, and global diastolic RV dysfunction, indirect signals of pulmonary arterial hypertension were shown by echocardiography, mostly evident in SHRSAD. The RV-EDP increased in all groups compared to W(W:3±0.39mmHg, *SAD:4.7±0.52mmHg, *SHR: 6.6±1.1mmHg, *SHRSAD:7.8±0.87mmHg, *p<0.05 vs. W), and LV-EDP increased in SHR and SHRSAD groups compared to W, and in SHRSAD compared to SAD (W: 5,83±0,19 mmHg,SAD: 8.98±1.2 mmHg, *SHR: 12.51±4.73 mmHg, *#SHRSAD: 14.57±2.52mmHg, *p<0.05vs.W,#p<0.05 vs. DSA). There was a relation between invasive or noninvasive measurements of RV showing good accuracy of echocardiographic measurements. Conclusions: Our results suggest that baroreflex dysfunction impaired biventricular function. Moreover, the findings of RV dysfunction indicate that SAD may lead to increased pulmonary artery pressure, supporting a role for baroreflex dysfunction in the pathogenesis of the hypertensive cardiac disease.- Cardiac dysfunction in Pkd1-deficient mice with phenotype rescue by galectin-3 knockout(2016) BALBO, Bruno E.; AMARAL, Andressa G.; FONSECA, Jonathan M.; CASTRO, Isac de; SALEMI, Vera M.; SOUZA, Leandro E.; SANTOS, Fernando dos; IRIGOYEN, Maria C.; QIAN, Feng; CHAMMAS, Roger; ONUCHIC, Luiz F.Alterations in myocardial wall texture stand out among ADPKD cardiovascular manifestations in hypertensive and normotensive patients. To elucidate their pathogenesis, we analyzed the cardiac phenotype in Pkd1(cond/cond) Nestin(cre) (CYG+) cystic mice exposed to increased blood pressure, at 5 to 6 and 20 to 24 weeks of age, and Pkd1(+/-) (HTG+) noncystic mice at 5-6 and 10-13 weeks. Echocardiographic analyses revealed decreased myocardial deformation and systolic function in CYG+ and HTG+ mice, as well as diastolic dysfunction in older CYG+ mice, compared to their Pkd1(cond/cond) and Pkd1(+/+) controls. Hearts from CYG+ and HTG+ mice presented reduced polycystin-1 expression, increased apoptosis, and mild fibrosis. Since galectin-3 has been associated with heart dysfunction, we studied it as a potential modifier of the ADPKD cardiac phenotype. Double-mutant Pkd1(cond/cond):Nestin(cre);Lgals(3-/-) (CYG-) and Pkd1(+/-);Lgals(3-/-) (HTG-) mice displayed improved cardiac deformability and systolic parameters compared to single -mutants, not differing from the controls. CYG- and HTG- showed decreased apoptosis and fibrosis. Analysis of a severe cystic model (Pkd1(v/v); VVG+) showed that Pkd1(v/v);Lgals(3-/-) (VVG-) mice have longer survival, decreased cardiac apoptosis and improved heart function compared to VVG+. CYG- and VVG- animals showed no difference in renal cystic burden compared to CYG+ and VVG+ mice. Thus, myocardial dysfunction occurs in different Pkdl-deficient models and suppression of galectin-3 expression rescues this phenotype.
- Smoking accelerates renal cystic disease and worsens cardiac phenotype in Pkd1-deficient mice(2021) SOUSA, Marciana V.; AMARAL, Andressa G.; FREITAS, Jessica A.; MURATA, Gilson M.; WATANABE, Elieser H.; BALBO, Bruno E.; TAVARES, Marcelo D.; HORTEGAL, Renato A.; ROCON, Camila; SOUZA, Leandro E.; IRIGOYEN, Maria C.; SALEMI, Vera M.; ONUCHIC, Luiz F.Smoking has been associated with renal disease progression in ADPKD but the underlying deleterious mechanisms and whether it specifically worsens the cardiac phenotype remain unknown. To investigate these matters, Pkd1-deficient cystic mice and noncystic littermates were exposed to smoking from conception to 18 weeks of age and, along with nonexposed controls, were analyzed at 13-18 weeks. Renal cystic index and cyst-lining cell proliferation were higher in cystic mice exposed to smoking than nonexposed cystic animals. Smoking increased serum urea nitrogen in cystic and noncystic mice and independently enhanced tubular cell proliferation and apoptosis. Smoking also increased renal fibrosis, however this effect was much higher in cystic than in noncystic animals. Pkd1 deficiency and smoking showed independent and additive effects on reducing renal levels of glutathione. Systolic function and several cardiac structural parameters were also negatively affected by smoking and the Pkd1-deficient status, following independent and additive patterns. Smoking did not increase, however, cardiac apoptosis or fibrosis in cystic and noncystic mice. Notably, smoking promoted a much higher reduction in body weight in Pkd1-deficient than in noncystic animals. Our findings show that smoking aggravated the renal and cardiac phenotypes of Pkd1-deficient cystic mice, suggesting that similar effects may occur in human ADPKD.
- Effects of sympathectomy on myocardium remodeling and function(2021) JORDAO, Mauricio Rodrigues; PESSOA, Fernanda G.; FONSECA, Keila C. B.; ZANONI, Fernando; SALEMI, Vera M. C.; SOUZA, Leandro E.; RIBEIRO, Orlando N.; FERNANDES, Fabio; IRIGOYEN, Maria Claudia; MOREIRA, Luiz Felipe P.; MADY, Charles; RAMIRES, Felix Jose AlvarezOBJECTIVES: To evaluate the effects of sympathectomy on the myocardium in an experimental model. METHODS: The study evaluated three groups of male Wistar rats: control (CT; n=15), left unilateral sympathectomy (UNI; n=15), and bilateral sympathectomy (BIL; n=31). Sympathectomy was performed by injection of absolute alcohol into the space of the spinous process of the C7 vertebra. After 6 weeks, we assessed the chronotropic properties at rest and stress, cardiovascular autonomic modulation, myocardial and peripheral catecholamines, and beta-adrenergic receptors in the myocardium. The treadmill test consisted of an escalated protocol with a velocity increment until the maximal velocity tolerated by the animal was reached. RESULTS: The bilateral group had higher levels of peripheral catecholamines, and consequently, a higher heart rate (HR) and blood pressure levels. This suggests that the activation of a compensatory pathway in this group may have deleterious effects. The BIL group had basal tachycardia immediately before the exercise test and increased tachycardia at peak exercise (p<0.01); the blood pressure had the same pattern (p=0.0365). The variables related to autonomic modulation were not significantly different between groups, with the exception of the high frequency (HF) variable, which showed significant differences in CT vs UNI. There was no significant difference in beta receptor expression between groups. There was a higher concentration of peripheral norepinephrine in the BIL group (p=0.0001), and no significant difference in myocardial norepinephrine (p=0.09). CONCLUSION: These findings suggest that an extra cardiac compensatory pathway increases the sympathetic tonus and maintains a higher HR and higher levels of peripheral catecholamines in the procedure groups. The increase in HF activity can be interpreted as an attempt to increase the parasympathetic tonus to balance the greater sympathetic activity.