Autonomic modulation of the electrical substrate in mice haploinsufficient for cardiac sodium channels: a model of the Brugada syndrome.
Am J Physiol Cell Physiol
; 317(3): C576-C583, 2019 09 01.
Article
em En
| MEDLINE
| ID: mdl-31291141
ABSTRACT
A murine line haploinsufficient in the cardiac sodium channel has been used to model human Brugada syndrome a disease causing sudden cardiac death due to lethal ventricular arrhythmias. We explored the effects of cholinergic tone on electrophysiological parameters in wild-type and genetically modified, heterozygous, Scn5a+/- knockout mice. Scn5a+/- ventricular slices showed longer refractory periods than wild-type both at baseline and during isoprenaline challenge. Scn5a+/- hearts also showed lower conduction velocities and increased mean increase in delay than did littermate controls at baseline and blunted responses to isoprenaline challenge. Carbachol exerted limited effects but reversed the effects of isoprenaline with coapplication. Scn5a+/- mice showed a reduction in conduction reserve in that isoprenaline no longer increased conduction velocity, and this was not antagonized by muscarinic agonists.
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MEDLINE
Assunto principal:
Síndrome de Brugada
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Haploinsuficiência
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Canal de Sódio Disparado por Voltagem NAV1.5
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Preparação de Coração Isolado
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Contração Miocárdica
Limite:
Animals
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article