Baroreflex and cardiac dysfunctions evaluated by transesophageal echocardiography, baroreflex sensitivity, autonomic control and invasive measurements in rats submitted to sinoaortic denervation
Nenhuma Miniatura disponível
Citações na Scopus
Tipo de produção
conferenceObject
Data de publicação
2012
Título da Revista
ISSN da Revista
Título do Volume
Editora
OXFORD UNIV PRESS
Autores
FUENTE, R. La
CANDIDO, G.
MEDEIROS, A.
Citação
EUROPEAN HEART JOURNAL, v.33, suppl.1, p.200-201, 2012
Resumo
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.