Linked Life Data

19471098

Source:http://linkedlifedata.com/resource/pubmed/id/19471098

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4-6
pubmed:dateCreated
2009-5-27
pubmed:abstractText
Despite prolongation of the QTc interval in humans during cerebral ischemia, little is known about the mechanisms that underlie these actions. Cerebral ischemic model was established by middle cerebral artery occlusion (MCAO) for 24 h. In rat ventricular myocytes, the effect of cerebral ischemia on action potential duration (APD) and underlying electrophysiologic mechanisms were investigated by whole-cell patch clamp. We demonstrated that heart rate-corrected QT interval and APD were prolonged with frequent occurrence of ventricular tachyarrhythmias in a rat model of MCAO. The I(Na) density was overall smaller in cerebral ischemic myocytes relative to sham myocytes (P < 0.01). The Nav1.5 protein and mRNA levels (pore-forming subunit for I(Na) ) were decreased by about 20% (P < 0.01) in cerebral ischemic rat hearts than those in sham-operated rat hearts. Peak transient outward K(+) current (I(to)) at +60 mV was found decreased by approximately 32.3% (P < 0.01) in cerebral ischemic rats. The peak amplitude of L-type Ca(2+) current (I(Ca,L)) was increased and the inactivation kinetics were slowed (P < 0.01). Protein level of the pore-forming subunit for I(to) was decreased, but that for I(Ca,L) was increased. The inward rectifier K(+) current (I(K1)) at -120 mV and its protein level were unaffected. Our study represents the first documentation of I(Na), I(to) and I(Ca,L) channelopathy as the major ionic mechanism for cerebral ischemic QT prolongation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1421-9778
pubmed:author
pubmed:copyrightInfo
Copyright 2009 S. Karger AG, Basel.
pubmed:issnType
Electronic
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
305-16
pubmed:dateRevised
2011-7-22
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Ionic mechanisms underlying action potential prolongation by focal cerebral ischemia in rat ventricular myocytes.
pubmed:affiliation
Department of Pharmacology, State-Province Key Laboratory of China, Heilongjiang, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't