Linked Life Data

2055235

Source:http://linkedlifedata.com/resource/pubmed/id/2055235

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1991-7-31
pubmed:abstractText
Electrophysiological effects of lysophosphatidylcholine (50 or 100 microM) and D,L-carnitine (100 microM) were studied under control conditions and in response to simulated ischaemia and reperfusion using the superfused right ventricular free wall preparation from the guinea pig heart. Lysophosphatidylcholine, 100 microM, induced a significant depolarization of the maximum diastolic potential (MDP) in the epicardium, as well as the development of ventricular premature beats, salvos and ventricular tachycardia. Both coupled beats and abnormal automaticity were observed in lysophosphatidylcholine (100 microM)-treated preparations. Carnitine (100 microM) alone had no effect on preparations superfused with normal Tyrode solution. However, it delayed the time to onset and reduced the cumulative duration of lysophosphatidylcholine-induced arrhythmias (P less than 0.05). The incidence of lysophosphatidylcholine-induced abnormal automaticity and salvos was also significantly decreased in the presence of carnitine. Twenty minutes of simulated ischaemia caused depolarization of MDP as well as prolongation followed by block of transmural conduction. Lysophosphatidylcholine (100 microM) did not alter this response however, carnitine significantly reduced ischaemia-induced depolarization in the epicardium. All control preparations developed arrhythmic activity during 30 min of reperfusion. Carnitine accelerated recovery of MDP in the epicardium upon reperfusion, prolonged the time to onset of arrhythmic activity and reduced both its cumulative duration and incidence. In contrast, reperfusion in the presence of lysophosphatidylcholine (100 microM) significantly increased the incidence of arrhythmic activity. Carnitine exerted only minimal antiarrhythmic action when preparations were exposed to reperfusion in the presence of lysophosphatidylcholine. In conclusion, this study demonstrates that carnitine can modify various cellular mechanisms of arrhythmia induced by lysophosphatidylcholine or by reperfusion but is much less effective when lysophosphatidylcholine and reperfusion are combined.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
17
pubmed:volume
192
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
355-63
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Protective effects of D,L-carnitine against arrhythmias induced by lysophosphatidylcholine or reperfusion.
pubmed:affiliation
Department of Pharmacology and Toxicology, University of Western Ontario, London, Canada.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't