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dc.contributor.authorEntz, Michael, IIen_US
dc.contributor.authorGeorge, Sharon A.en_US
dc.contributor.authorZeitz, Michael J.en_US
dc.contributor.authorRaisch, Tristanen_US
dc.contributor.authorSmyth, James W.en_US
dc.contributor.authorPoelzing, Stevenen_US
dc.date.accessioned2017-02-03T15:09:32Z
dc.date.available2017-02-03T15:09:32Z
dc.date.issued2016-02-02en_US
dc.identifier.issn1664-042Xen_US
dc.identifier.urihttp://hdl.handle.net/10919/74920
dc.description.abstractBackground: Recent studies suggested that cardiac conduction in murine hearts with narrow perinexi and 50% reduced connexin43 (Cx43) expression is more sensitive to relatively physiological changes of extracellular potassium ([K+](o)) and sodium ([Na+](o)). Purpose: Determine whether similar [K+](o) and [Na+](o) changes alter conduction velocity (CV) sensitivity to pharmacologic gap junction (GJ) uncoupling in guinea pigs. Methods: [K+](o) and [Na+](o) were varied in Langendorff perfused guinea pig ventricles (Solution A: [K+](o) = 4.56 and [N+](o) = 153.3 mM. Solution B: [K+](o) = 6.95 and [Na+](o) = 145.5 mM). Gap junctions were inhibited with carbenoxolone (CBX) (15 and 30 mu M). Epicardial CV was quantified by optical mapping. Perinexal width was measured with transmission electron microscopy. Total and phosphorylated Cx43 were evaluated by western blotting. Results: Solution composition did not alter CV under control conditions or with 15 mu M CBX. Decreasing the basic cycle length (BCL) of pacing from 300 to 160 ms decreased CV uniformly with both solutions. At 30 mu M CBX, a change in solution did not alter CV either longitudinally or transversely at BCL = 300 ms. However, reducing BCL to 160 ms caused CV to decrease more in hearts perfused with Solution B than A. Solution composition did not alter perinexal width, nor did it change total or phosphorylated serine 368 Cx43 expression. These data suggest that the solution dependent CV changes were independent of altered perinexal width or GJ coupling. Action potential duration was always shorter in hearts perfused with Solution B than A. independent of pacing rate and/or CBX concentration. Conclusions: Increased heart rate and GJ uncoupling can unmask small CV differences caused by changing [K+](o) and [Na+](o). These data suggest that modulating extracellular ionic composition may be a novel anti-arrhythmic target in diseases with abnormal GJ coupling, particularly when heart rate cannot be controlled.en
dc.format.extent? - ? (10) page(s)en_US
dc.languageEnglishen_US
dc.publisherFrontiersen_US
dc.relation.urihttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000369058400001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=930d57c9ac61a043676db62af60056c1en_US
dc.rightsCreative Commons Attribution 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectPhysiologyen_US
dc.subjectelectrophysiologyen_US
dc.subjectcardiac conductionen_US
dc.subjectephaptic couplingen_US
dc.subjectgap junctionen_US
dc.subjectALTERED CONNEXIN43 EXPRESSIONen_US
dc.subjectCARDIAC CONDUCTIONen_US
dc.subjectIMPULSE PROPAGATIONen_US
dc.subjectPURKINJE-FIBERSen_US
dc.subjectMECHANISMSen_US
dc.subjectMODELen_US
dc.subjectISCHEMIAen_US
dc.subjectVELOCITYen_US
dc.subjectCELLSen_US
dc.subjectHEMICHANNELSen_US
dc.titleHeart Rate and Extracellular Sodium and Potassium Modulation of Gap Junction Mediated Conduction in Guinea Pigsen_US
dc.typeArticle - Refereed
dc.description.versionPublished (Publication status)en_US
dc.title.serialFrontiers in Physiologyen_US
dc.identifier.doihttps://doi.org/10.3389/fphys.2016.00016
dc.identifier.volume7en_US
pubs.organisational-group/Virginia Tech
pubs.organisational-group/Virginia Tech/All T&R Faculty
pubs.organisational-group/Virginia Tech/Faculty of Health Sciences
pubs.organisational-group/Virginia Tech/University Research Institutes
pubs.organisational-group/Virginia Tech/University Research Institutes/Virginia Tech Carilion Research Institute


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Creative Commons Attribution 4.0 International
License: Creative Commons Attribution 4.0 International