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Article: Transmural action potential and ionic current remodeling in ventricles of failing canine hearts

TitleTransmural action potential and ionic current remodeling in ventricles of failing canine hearts
Authors
Issue Date2002
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 2002, v. 283 n. 3 52-3, p. H1031-H1041 How to Cite?
AbstractHeart failure (HF) produces important alterations in currents underlying cardiac repolarization, but the transmural distribution of such changes is unknown. We therefore recorded action potentials and ionic currents in cells isolated from the endocardium, midmyocardium, and epicardium of the left ventricle from dogs with and without tachypacing-induced HF. HF greatly increased action potential duration (APD) but attenuated APD heterogeneity in the three regions. Early afterdepolarizations (EADs) were observed in all cell types of failing hearts but not in controls. Inward rectifier K + current (I K1) was homogeneously reduced by ∼41% (at -60 mV) in the three cell types. Transient outward K+ current (I to1) was decreased by 43-45% at +30 mV, and the slow component of the delayed rectifier K + current (I to1) was significantly downregulated by 57%, 49%, and 58%, respectively, in epicardial, midmyocardial, and endocardial cells, whereas the rapid component of the delayed rectifier K + current was not altered. The results indicate that HF remodels electrophysiology in all layers of the left ventricle, and the downregulation of I K1, I to1 and I Ks increases APD and favors occurrence of EADs.
Persistent Identifierhttp://hdl.handle.net/10722/78021
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, GRen_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorDucharme, Aen_HK
dc.contributor.authorTardif, JCen_HK
dc.contributor.authorNattel, Sen_HK
dc.date.accessioned2010-09-06T07:38:18Z-
dc.date.available2010-09-06T07:38:18Z-
dc.date.issued2002en_HK
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2002, v. 283 n. 3 52-3, p. H1031-H1041en_HK
dc.identifier.issn0363-6135en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78021-
dc.description.abstractHeart failure (HF) produces important alterations in currents underlying cardiac repolarization, but the transmural distribution of such changes is unknown. We therefore recorded action potentials and ionic currents in cells isolated from the endocardium, midmyocardium, and epicardium of the left ventricle from dogs with and without tachypacing-induced HF. HF greatly increased action potential duration (APD) but attenuated APD heterogeneity in the three regions. Early afterdepolarizations (EADs) were observed in all cell types of failing hearts but not in controls. Inward rectifier K + current (I K1) was homogeneously reduced by ∼41% (at -60 mV) in the three cell types. Transient outward K+ current (I to1) was decreased by 43-45% at +30 mV, and the slow component of the delayed rectifier K + current (I to1) was significantly downregulated by 57%, 49%, and 58%, respectively, in epicardial, midmyocardial, and endocardial cells, whereas the rapid component of the delayed rectifier K + current was not altered. The results indicate that HF remodels electrophysiology in all layers of the left ventricle, and the downregulation of I K1, I to1 and I Ks increases APD and favors occurrence of EADs.en_HK
dc.languageengen_HK
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_HK
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_HK
dc.subject.meshAction Potentials - physiologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshArrhythmias, Cardiac - physiopathologyen_HK
dc.subject.meshCalcium - metabolismen_HK
dc.subject.meshCalcium Channels, L-Type - physiologyen_HK
dc.subject.meshDogsen_HK
dc.subject.meshEndocardium - physiopathologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHeart Failure - physiopathologyen_HK
dc.subject.meshHeart Ventricles - physiopathologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshPatch-Clamp Techniquesen_HK
dc.subject.meshPotassium - metabolismen_HK
dc.subject.meshPotassium Channels, Inwardly Rectifying - physiologyen_HK
dc.subject.meshVentricular Remodeling - physiologyen_HK
dc.titleTransmural action potential and ionic current remodeling in ventricles of failing canine heartsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0363-6135&volume=283&issue=3&spage=H1031&epage=41&date=2002&atitle=Transmural+action+potential+and+ionic+current+remodeling+in+ventricles+of+failing+canine+hearts.++++en_HK
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_HK
dc.identifier.authorityLi, GR=rp00476en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1152/ajpheart.00105.2002-
dc.identifier.pmid12181133-
dc.identifier.scopuseid_2-s2.0-0036352059en_HK
dc.identifier.hkuros139468en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036352059&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume283en_HK
dc.identifier.issue3 52-3en_HK
dc.identifier.spageH1031en_HK
dc.identifier.epageH1041en_HK
dc.identifier.isiWOS:000177502200024-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, GR=7408462932en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.scopusauthoridDucharme, A=7003600209en_HK
dc.identifier.scopusauthoridTardif, JC=35399980400en_HK
dc.identifier.scopusauthoridNattel, S=36947837400en_HK

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