Linked Life Data

17626898

Source:http://linkedlifedata.com/resource/pubmed/id/17626898

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-8-31
pubmed:abstractText
Previous studies have shown that the gating kinetics of the slow component of the delayed rectifier K(+) current (I(Ks)) contribute to postrepolarization refractoriness in isolated cardiomyocytes. However, the impact of such kinetics on arrhythmogenesis remains unknown. We surmised that expression of I(Ks) in rat cardiomyocyte monolayers contributes to wavebreak formation and facilitates fibrillatory conduction by promoting postrepolarization refractoriness. Optical mapping was performed in 44 rat ventricular myocyte monolayers infected with an adenovirus carrying the genomic sequences of KvLQT1 and minK (molecular correlates of I(Ks)) and 41 littermate controls infected with a GFP adenovirus. Repetitive bipolar stimulation was applied at increasing frequencies, starting at 1 Hz until loss of 1:1 capture or initiation of reentry. Action potential duration (APD) was significantly shorter in I(Ks)-infected monolayers than in controls at 1 to 3 Hz (P<0.05), whereas differences at higher pacing frequencies did not reach statistical significance. Stable rotors occurred in both groups, with significantly higher rotation frequencies, lower conduction velocities, and shorter action potentials in the I(Ks) group. Wavelengths in the latter were significantly shorter than in controls at all rotation frequencies. Wavebreaks leading to fibrillatory conduction occurred in 45% of the I(Ks) reentry episodes but in none of the controls. Moreover, the density of wavebreaks increased with time as long as a stable source sustained the fibrillatory activity. These results provide the first demonstration that I(Ks)-mediated postrepolarization refractoriness can promote wavebreak formation and fibrillatory conduction during pacing and sustained reentry and may have important implications in tachyarrhythmias.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
31
pubmed:volume
101
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
475-83
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:17626898-Action Potentials, pubmed-meshheading:17626898-Adenoviridae, pubmed-meshheading:17626898-Animals, pubmed-meshheading:17626898-Animals, Newborn, pubmed-meshheading:17626898-Arrhythmias, Cardiac, pubmed-meshheading:17626898-Cells, Cultured, pubmed-meshheading:17626898-DNA, Complementary, pubmed-meshheading:17626898-Electrophysiology, pubmed-meshheading:17626898-Heart Conduction System, pubmed-meshheading:17626898-Heart Ventricles, pubmed-meshheading:17626898-KCNQ1 Potassium Channel, pubmed-meshheading:17626898-Myocytes, Cardiac, pubmed-meshheading:17626898-Potassium Channels, Voltage-Gated, pubmed-meshheading:17626898-Rats, pubmed-meshheading:17626898-Rats, Sprague-Dawley, pubmed-meshheading:17626898-Receptors, Adrenergic, beta, pubmed-meshheading:17626898-Ventricular Function
pubmed:year
2007
pubmed:articleTitle
Adenoviral expression of IKs contributes to wavebreak and fibrillatory conduction in neonatal rat ventricular cardiomyocyte monolayers.
pubmed:affiliation
Department of Pharmacology, SUNY Upstate Medical University, Syracuse, NY 13210, USA. munozv@upstate.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural