Linked Life Data

11911222

Source:http://linkedlifedata.com/resource/pubmed/id/11911222

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-3-25
pubmed:abstractText
Selective blockade of the inward rectifier potassium channel I(K1) by barium, or of the rapidly activating delayed rectifier potassium channel I(Kr) by D,L-sotalol, prolongs repolarization and reduces the defibrillation threshold (DFT). This study hypothesized that combination I(K1) and I(Kr) channel block would produce concentration-dependent additive effects on DFT and ventricular refractoriness. A range of barium and D,L-sotalol concentrations, alone and in combination, were examined with respect to DFT, ventricular effective refractory period (VERP), and ventricular fibrillation cycle length (VFCL) in 133 Langendorff-perfused rabbit hearts. Barium produced a concentration-dependent reduction of DFT (-49+/-4%), with concentration-dependent increases in VERP (26+/-6%) and VFCL (42+/-18%). D,L-Sotalol produced a concentration-dependent lowering of DFT (-53+/-6%) with a concentration-dependent increase in VFCL (34+/-8%) but not VERP. Low (1.6 microM), intermediate (3.1 microM), and high (12.5 microM) barium concentrations combined with varying D,L-sotalol concentrations produced equal or smaller decreases in DFT compared with corresponding doses of barium or D,L-sotalol alone. Except at the lowest concentrations of barium (1.6 and 3.1 microM) (p < 0.05), there was no significant additive interaction between barium and D,L-sotalol on VERP or VFCL. Combination I(K1) and I(Kr) channel block by barium and D,L-sotalol does not produce additive reduction of DFT.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0008-4212
pubmed:author
pubmed:issnType
Print
pubmed:volume
80
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
22-30
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11911222-Algorithms, pubmed-meshheading:11911222-Animals, pubmed-meshheading:11911222-Anti-Arrhythmia Agents, pubmed-meshheading:11911222-Barium, pubmed-meshheading:11911222-Delayed Rectifier Potassium Channels, pubmed-meshheading:11911222-Dose-Response Relationship, Drug, pubmed-meshheading:11911222-Electric Countershock, pubmed-meshheading:11911222-Electrophysiology, pubmed-meshheading:11911222-Heart Function Tests, pubmed-meshheading:11911222-Male, pubmed-meshheading:11911222-Potassium Channel Blockers, pubmed-meshheading:11911222-Potassium Channels, pubmed-meshheading:11911222-Potassium Channels, Inwardly Rectifying, pubmed-meshheading:11911222-Potassium Channels, Voltage-Gated, pubmed-meshheading:11911222-Rabbits, pubmed-meshheading:11911222-Refractory Period, Electrophysiological, pubmed-meshheading:11911222-Sotalol
pubmed:year
2002
pubmed:articleTitle
Combination IK1 and IKr channel blockade: no additive lowering of the defibrillation threshold.
pubmed:affiliation
Department of Pharmacology, University of Toronto, ON, Canada.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't