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Acute vagal modulation of electrophysiology of the atrial and pulmonary veins increases vulnerability to atrial fibrillation

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dc.contributor.authorOliveira, Mario
dc.contributor.authorda Silva, M. Nogueira
dc.contributor.authorGeraldes, Vera
dc.contributor.authorXavier, Rita
dc.contributor.authorLaranjo, Sergio
dc.contributor.authorSilva, Vitor
dc.contributor.authorPostolache, Gabriela
dc.contributor.authorFerreira, Rui
dc.contributor.authorRocha, Isabel
dc.date.accessioned2023-04-27T10:38:52Z
dc.date.available2023-04-27T10:38:52Z
dc.date.issued2011
dc.description© 2010 The Authors. Journal compilation © 2011 The Physiological Societypt_PT
dc.description.abstractVagal activity is thought to influence atrial electrophysiological properties and play a role in the initiation and maintenance of atrial fibrillation (AF). We evaluated the effects of acute vagal stimulation on atrial conduction, refractoriness of atrial and pulmonary veins (PVs) and inducibility of AF. An open-chest epicardial approach was performed in New Zealand White rabbits with preserved autonomic innervation. Atrial electrograms were obtained with four unipolar electrodes placed epicardially along the atria (n = 22) and an electrode adapted to the proximal left PV (n = 10). The cervical vagus nerve was stimulated with bipolar platinum electrodes (20 Hz). Epicardial activation was recorded in sinus rhythm, and effective refractory periods (ERPs), dispersion of refractoriness and conduction times from high-lateral right atrium (RA) to high-lateral left atrium (LA) and PVs assessed at baseline and during vagal stimulation. Burst pacing (50 Hz, 10 s), alone or combined with vagal stimulation, was applied to the right (RAA) and left atrial appendage (LAA) and PVs to induce AF. At baseline, ERPs were lower in PVs than in LA and LAA, but did not differ significantly from RA and RAA, and there was a significant delay in the conduction time from RA to PVs compared with the activation time from RA to LA (P < 0.01). During vagal stimulation, ERP decreased significantly at all sites, without significant differences in the dispersion of refractoriness, and the atrial conduction times changed from 39 ± 19 to 49 ± 9 ms (RA to PVs; n.s.) and from 14 ± 7 to 28 ± 12 ms (RA to LA; P = 0.01). Induction of AF was reproducible in 50% of cases with 50 Hz and in 82% with 50 Hz combined with vagal stimulation (P < 0.05). During vagal stimulation, AF cycle length decreased at all sites, and AF duration changed from 1.0 ± 0.9 to 14.0 ± 10.0 s (P < 0.01), with documentation of PV tachycardia in three cases. In 70% of the animals, AF ceased immediately after interruption of vagal stimulation. We conclude that in the intact rabbit heart, vagal activity prolongs interatrial conduction and shortens atrial and PV ERP, contributing to the vulnerability to the induction and maintenance of AF. This model may be useful in the assessment of the autonomic influence in the mechanisms underlying AF.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationExp Physiol. 2011 Feb;96(2):125-133pt_PT
dc.identifier.doi10.1113/expphysiol.2010.053280pt_PT
dc.identifier.eissn1469-445X
dc.identifier.issn0958-0670
dc.identifier.urihttp://hdl.handle.net/10451/57268
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherWileypt_PT
dc.relation.publisherversionhttps://physoc.onlinelibrary.wiley.com/journal/1469445xpt_PT
dc.titleAcute vagal modulation of electrophysiology of the atrial and pulmonary veins increases vulnerability to atrial fibrillationpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage133pt_PT
oaire.citation.issue2pt_PT
oaire.citation.startPage125pt_PT
oaire.citation.titleExperimental Physiologypt_PT
oaire.citation.volume96pt_PT
person.familyNameMartins Oliveira
person.familyNameGeraldes
person.familyNameLaranjo
person.familyNamePostolache
person.familyNamerocha
person.givenNameMario Joao
person.givenNameVera
person.givenNameSergio
person.givenNameGabriela
person.givenNameisabel
person.identifier36332
person.identifier.ciencia-id2312-2190-19B2
person.identifier.ciencia-idD51D-E96C-1633
person.identifier.ciencia-id351B-92E1-0C50
person.identifier.orcid0000-0002-8371-8354
person.identifier.orcid0000-0003-1275-3459
person.identifier.orcid0000-0003-2169-4024
person.identifier.orcid0000-0002-3052-1232
person.identifier.orcid0000-0002-7582-0893
person.identifier.ridM-4137-2013
person.identifier.ridG-2909-2011
person.identifier.scopus-author-id24391148400
person.identifier.scopus-author-id6506875525
rcaap.rightsrestrictedAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublication81e0b444-8832-47a8-a911-2f89eb33545d
relation.isAuthorOfPublication16b49724-d060-4106-955d-d211cba44c12
relation.isAuthorOfPublication902d64d7-c6bf-4b05-8f49-3b52dd0aa452
relation.isAuthorOfPublicatione25cdee0-555e-42b4-b33a-c349dfe4a963
relation.isAuthorOfPublication472714e8-fa6c-4d7b-9c4d-d6f5b55e39f4
relation.isAuthorOfPublication.latestForDiscovery16b49724-d060-4106-955d-d211cba44c12

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