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

A. Farkas, Susan J. Coker

Research output: Contribution to journalArticle

9 Citations (Scopus)

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).
Original languageEnglish
Pages (from-to)189-196
Number of pages8
JournalEuropean Journal of Pharmacology
Volume472
Issue number3
DOIs
Publication statusPublished - 2003

Keywords

  • torsade de pointes
  • proarrhythmia
  • QT prolongation
  • prostaglandin E2
  • K+ channel
  • ATP-dependent

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