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Article: Ionic remodeling underlying action potential changes in a canine model of atrial fibrillation

TitleIonic remodeling underlying action potential changes in a canine model of atrial fibrillation
Authors
Issue Date1997
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1997, v. 81 n. 4, p. 512-525 How to Cite?
AbstractRapid electrical activation, as occurs during atrial fibrillation (AF), is known to cause reductions in atrial refractoriness and in adaptation to heart rate of the atrial refractory period, which promote the maintenance of AF, but the underlying ionic mechanisms are unknown. In order to determine the cellular and ionic changes caused by chronic atrial tachycardia, we studied right atrial myocytes from dogs subjected to 1, 7, or 42 days of atrial pacing at 400/min and compared them with myocytes from sham-operated dogs (pacemaker inserted but not activated). Rapid pacing led to progressive increases in the duration of AF induced by bursts of 10-Hz stimuli (from 3±2 seconds in sham-operated dogs to 3060±707 seconds in dogs after 42 days of pacing, P<.001) and reduced atrial refractoriness and adaptation to rate of the atrial refractory period. Voltage-damp studies showed that chronic rapid pacing did not alter inward rectifier K + current, rapid or slow components of the delayed rectifier current, the ultrarapid delayed rectifier current, T-type Ca 2+ current, or Ca 2+-dependent Cl - current. In contrast, the densities of transient outward current (I(lo)) and L-type Ca 2+ current (I(Ca))were progressively reduced as the duration of rapid pacing increased, without concomitant changes in kinetics or voltage dependence. In keeping with in vivo changes in refractoriness, action potential duration (APD) and APD adaptation to rate were decreased by rapid pacing. The response of the action potential and ionic currents flowing during the action potential (as exposed by action-potential voltage clamp) to nifedipine in normal canine cells and in cells from rapidly paced dogs suggested that the APD changes in paced dogs were largely due to reductions in I(Ca). We conclude that sustained atrial tachycardia reduces I(lo) and I(Ca), that the reduced I(Ca) decreases APD and APD adaptation to rate, and that these cellular changes likely account for the alterations in atrial refractoriness associated with enhanced ability to maintain AF in the model.
Persistent Identifierhttp://hdl.handle.net/10722/162179
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYue, Len_US
dc.contributor.authorFeng, Jen_US
dc.contributor.authorGaspo, Ren_US
dc.contributor.authorLi, GRen_US
dc.contributor.authorWang, Zen_US
dc.contributor.authorNattel, Sen_US
dc.date.accessioned2012-09-05T05:17:51Z-
dc.date.available2012-09-05T05:17:51Z-
dc.date.issued1997en_US
dc.identifier.citationCirculation Research, 1997, v. 81 n. 4, p. 512-525en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/162179-
dc.description.abstractRapid electrical activation, as occurs during atrial fibrillation (AF), is known to cause reductions in atrial refractoriness and in adaptation to heart rate of the atrial refractory period, which promote the maintenance of AF, but the underlying ionic mechanisms are unknown. In order to determine the cellular and ionic changes caused by chronic atrial tachycardia, we studied right atrial myocytes from dogs subjected to 1, 7, or 42 days of atrial pacing at 400/min and compared them with myocytes from sham-operated dogs (pacemaker inserted but not activated). Rapid pacing led to progressive increases in the duration of AF induced by bursts of 10-Hz stimuli (from 3±2 seconds in sham-operated dogs to 3060±707 seconds in dogs after 42 days of pacing, P<.001) and reduced atrial refractoriness and adaptation to rate of the atrial refractory period. Voltage-damp studies showed that chronic rapid pacing did not alter inward rectifier K + current, rapid or slow components of the delayed rectifier current, the ultrarapid delayed rectifier current, T-type Ca 2+ current, or Ca 2+-dependent Cl - current. In contrast, the densities of transient outward current (I(lo)) and L-type Ca 2+ current (I(Ca))were progressively reduced as the duration of rapid pacing increased, without concomitant changes in kinetics or voltage dependence. In keeping with in vivo changes in refractoriness, action potential duration (APD) and APD adaptation to rate were decreased by rapid pacing. The response of the action potential and ionic currents flowing during the action potential (as exposed by action-potential voltage clamp) to nifedipine in normal canine cells and in cells from rapidly paced dogs suggested that the APD changes in paced dogs were largely due to reductions in I(Ca). We conclude that sustained atrial tachycardia reduces I(lo) and I(Ca), that the reduced I(Ca) decreases APD and APD adaptation to rate, and that these cellular changes likely account for the alterations in atrial refractoriness associated with enhanced ability to maintain AF in the model.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_US
dc.relation.ispartofCirculation Researchen_US
dc.subject.meshAction Potentialsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAtrial Fibrillation - Metabolism - Physiopathologyen_US
dc.subject.meshAtrial Functionen_US
dc.subject.meshCalcium - Physiologyen_US
dc.subject.meshCardiac Pacing, Artificialen_US
dc.subject.meshChlorides - Physiologyen_US
dc.subject.meshDisease Susceptibilityen_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Conductivityen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshHeart - Physiopathologyen_US
dc.subject.meshIonsen_US
dc.subject.meshMyocardium - Metabolismen_US
dc.subject.meshPotassium - Physiologyen_US
dc.subject.meshTime Factorsen_US
dc.titleIonic remodeling underlying action potential changes in a canine model of atrial fibrillationen_US
dc.typeArticleen_US
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_US
dc.identifier.authorityLi, GR=rp00476en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid9314832en_US
dc.identifier.scopuseid_2-s2.0-0030765569en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030765569&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume81en_US
dc.identifier.issue4en_US
dc.identifier.spage512en_US
dc.identifier.epage525en_US
dc.identifier.isiWOS:A1997XZ01200008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYue, L=7101974873en_US
dc.identifier.scopusauthoridFeng, J=7403884361en_US
dc.identifier.scopusauthoridGaspo, R=6603283635en_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US
dc.identifier.scopusauthoridWang, Z=7410039597en_US
dc.identifier.scopusauthoridNattel, S=36048738800en_US

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