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Prevention of clofilium-induced torsade de pointes by prostaglandin E2 does not involve ATP-dependent k+ channels

Farkas, A. and Coker, Susan J. (2003) Prevention of clofilium-induced torsade de pointes by prostaglandin E2 does not involve ATP-dependent k+ channels. European Journal of Pharmacology, 472 (3). pp. 189-196. ISSN 0014-2999

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Abstract

Drugs that prolong the QT interval can trigger the life-threatening arrhythmia, torsade de pointes, but there is a poor correlation between the extent of QT prolongation and the occurrence of torsade de pointes. The clinical status of a patient may modify the arrhythmogenicity of drugs; thus, we have investigated whether a mediator of fever and inflammation, prostaglandin E2, alters the proarrhythmic effects of clofilium. In pentobarbitone-anaesthetized, open-chest, α-adrenoceptor-stimulated rabbits, prostaglandin E2 0.28, 0.84 and 2.80 nmol kg−1 min−1, infused into the left ventricle, reduced the incidence of torsade de pointes from 50% in controls to 20%, 20% and 0%, respectively (n=10 per group). Pretreatment with glibenclamide (10 μmol kg−1) did not alter the antiarrhythmic effect of prostaglandin E2 (2.80 nmol kg−1 min−1). These results indicate that prostaglandin E2 prevents drug-induced torsade de pointes and that this action of prostaglandin E2 is not mediated via opening of ATP-dependent K+ channels (KATP).

Item type: Article
ID code: 37990
Keywords: torsade de pointes, proarrhythmia, QT prolongation, prostaglandin E2, K+ channel, ATP-dependent , Pharmacy and materia medica, Pharmacology
Subjects: Medicine > Pharmacy and materia medica
Department: Faculty of Science > Strathclyde Institute of Pharmacy and Biomedical Sciences
Related URLs:
    Depositing user: Pure Administrator
    Date Deposited: 28 Feb 2012 16:23
    Last modified: 04 Sep 2014 19:16
    URI: http://strathprints.strath.ac.uk/id/eprint/37990

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