Modulação autonômica cardíaca no modelo murino da Síndrome de Down - Ts65Dn

Introduction: The Ts65Dn mouse is the most widely used animal model of Down syndrome (DS). Differences in autonomic regulation of heart rate variability (HRV) in individuals with DS have been hypothesized. Pharmacological studies in animal models may help us understand mechanisms underlying observed...

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Detalhes bibliográficos
Autor: Roque, Adriano Luis [UNIFESP]
Formato: tesis doctoral
Estado:Versión publicada
Fecha de publicación:2019
País:Brasil
Recursos:Universidade Federal de São Paulo (UNIFESP)
Repositorio:Repositório Institucional da UNIFESP
Idioma:portugués
OAI Identifier:oai:repositorio.unifesp.br:11600/59220
Acesso em linha:https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=8148837
https://repositorio.unifesp.br/handle/11600/59220
Access Level:acceso abierto
Palavra-chave:Heart Rate
Down Syndrome
Autonomic Nervous System
Cardiovascular System
Animal Models
Ts65Dn
Frequência Cardíaca
Síndrome De Down
Sistema Nervoso Autônomo
Sistema Cardiovascular
Modelos Animais
Descrição
Resumo:Introduction: The Ts65Dn mouse is the most widely used animal model of Down syndrome (DS). Differences in autonomic regulation of heart rate variability (HRV) in individuals with DS have been hypothesized. Pharmacological studies in animal models may help us understand mechanisms underlying observed changes in HRV in people with DS. Objective: Characterize cardiac autonomic modulation in a mouse model of Down Syndrome. Method: We recorded electrocardiograms (ECGs) from 10 Ts65Dn and 10 euploid control mice. For analysis of the data, we considered 30 minutes of baseline, followed by injection of adrenergic (isoproterenol) or cholinergic (carbachol) agonists.HRV analysis was performed using linear indices in time domain. Results and Discussion: Our results allow us to raise other hypotheses that may be evaluated in future studies, the amount of drug-degrading enzymes present in these mice, the sensitivity of the animals to these chemicals, the amount of adrenergic and cholinergic receptors of the Ts65Dn mice. Ts65Dn mice showed a possible overexpression of the GIRK2 gene and it seems to have increased cholinergic response and, consequently explaining the increase in heart rate variability found in these mice models of DS Conclusion: Ts65Dn mice presents deficits in cardiac autonomic modulation when compared with the euploid control group, mainly due to the reduction of indices related to global modulation (SD2 and SDNN).