Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/12650
Title: Cardiac Microvascular Rarefaction in Hyperthyroidism Induced Left Ventricle Dysfunction
Authors: Freitas, Felipe
Estato, Vanessa
Carvalho, Vinícius Frias
Torres, Rafael Carvalho
Lessa, Marcos Adriano
Tibiriçá, Eduardo
Affilliation: Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Investigação Cardiovascular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Investigação Cardiovascular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Inflamação. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Inflamação. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Investigação Cardiovascular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Investigação Cardiovascular. Rio de Janeiro, RJ, Brasil.
Abstract: Objective: The pathophysiology underlying hyperthyroidisminduced left ventricle (LV) dysfunction and hypertrophy directly involves the heart and indirectly involves the neuroendocrine systems. The effects of hyperthyroidism on the microcirculation are still controversial in experimental models. We investigated the effects of hyperthyroidism on the cardiac function and microcirculation of an experimental rat model. Methods: Male Wistar rats (170–250 g) were divided into two groups: the euthyroid group (n = 10), which was treated with 0.9% saline solution, and the hyperthyroid group (n = 10), which was treated with L-thyroxine (600 lg/kg/day, i.p.) during 14 days. An echocardiographic study was performed to evaluate the alterations in cardiac function, structure and geometry. The structural capillary density and the expression of angiotensin II AT1 receptor in the LV were analyzed using histochemistry and immunohistochemistry, respectively. Results: Hyperthyroidism was found to induce profound cardiovascular alterations, such as systolic hypertension, tachycardia, LV dysfunction, cardiac hypertrophy, and myocardial fibrosis. This study demonstrates the existence of structural capillary rarefaction and the down-regulation of the cardiac angiotensin II AT1 receptor in the myocardium of hyperthyroid rats in comparison with euthyroid rats. Conclusions: Microvascular rarefaction may be involved in the pathophysiology of hyperthyroidism-induced cardiovascular alterations.
Keywords: Experimental hyperthyroidism
Myocardial microcirculation
Left ventricular dysfunction
Cardiac fibrosis
keywords: Fibrose cardíaca
DeCS: Disfunção Ventricular Esquerda
Hipertireoidismo
Issue Date: 2013
Publisher: Wiley
Citation: FREITAS, Felipe; et al. Cardiac Microvascular Rarefaction in HyperthyroidismInduced Left Ventricle Dysfunction, v.20, n.7, p.590-598, Oct. 2013
DOI: 10.1111/micc.12057
ISSN: 1073-9688
Copyright: restricted access
Appears in Collections:IOC - Artigos de Periódicos

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