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Catecholaminergic effects on ventricular repolarization during inhibition of the rapid component of the delayed

Brian R Overholser1, Xiaomei Zheng, James E Tisdale

  • 1Department of Pharmacy Practice, School of Pharmacy and Pharmaceutical Sciences, Purdue University, West Lafayette, Indiana 46202, USA. boverhol@purdue.edu

Pharmacotherapy
|October 30, 2008
PubMed

Insights

Catecholamines prolonged ventricular repolarization during inhibition of the rapid component of the delayed rectifier potassium current (I(Kr)). This suggests counteracting mechanisms may contribute to an arrhythmogenic substrate during adrenergic activation with I(Kr) inhibition.

Area of Science:

  • Cardiovascular Physiology
  • Electrophysiology
  • Pharmacology

Background:

  • The rapid component of the delayed rectifier potassium current (I(Kr)) is crucial for ventricular repolarization.
  • Inhibition of I(Kr) is associated with QT prolongation and increased risk of arrhythmias.
  • Catecholamines influence cardiac electrophysiology through adrenergic receptors.

Purpose of the Study:

  • To investigate the effects of catecholamines on ventricular repolarization.
  • To determine these effects specifically during inhibition of I(Kr).

Main Methods:

  • Isolated perfused guinea pig heart model.
  • Administration of sparfloxacin to inhibit I(Kr).
  • Infusion of catecholamine admixtures (epinephrine and norepinephrine) during I(Kr) inhibition.
  • Measurement of left ventricular action potential duration (APD) at 90% and 30% repolarization (APD(90) and APD(30)).

Main Results:

  • Sparfloxacin administration significantly increased APD(90) and APD(30).
  • Subsequent catecholamine infusions during I(Kr) inhibition further increased APD(90) and APD(30).
  • A statistically significant net prolongation of ventricular repolarization was observed.

Conclusions:

  • Catecholamines cause a net prolongation of ventricular repolarization when I(Kr) is partially inhibited.
  • This finding suggests that counteracting mechanisms are activated.
  • These mechanisms may contribute to an arrhythmogenic substrate during adrenergic activation in the context of I(Kr) inhibition.
Abstract

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