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BJA Advance Access originally published online on September 24, 2007
British Journal of Anaesthesia 2007 99(5):726-733; doi:10.1093/bja/aem263
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© The Board of Management and Trustees of the British Journal of Anaesthesia 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Effects of articaine on action potential characteristics and the underlying ion currents in canine ventricular myocytes

A. Szabó1, N. Szentandrássy2, P. Birinyi2, B. Horváth2, G. Szabó2, T. Bányász2, I. Márton1, P. P. Nánási2,* and J. Magyar2

1 Department of Dentistry
2 Department of Physiology, Medical and Health Science Center, University of Debrecen, PO Box 22, 4012 Debrecen, Hungary

* Corresponding author. E-mail: nanasi{at}phys.dote.hu

Background: In spite of its widespread clinical application, there is little information on the cellular cardiac effects of articaine. In the present study, the concentration-dependent effects of articaine on action potential morphology and the underlying ion currents were studied in isolated canine ventricular cardiomyocytes.

Methods: Action potentials were recorded from the enzymatically dispersed myocytes using sharp microelectrodes (16 cells from 3 dogs). Conventional patch clamp and action potential voltage clamp arrangements were used to study the effects of articaine on transmembrane ion currents (37 cells from 14 dogs).

Results: Articaine-induced concentration-dependent changes in action potential configuration including shortening of the action potentials, reduction of their amplitude and maximum velocity of depolarization (Vmax), suppression of early repolarization and depression of plateau. The EC50 value obtained for the Vmax block was 162 (SD 30) µM. Both the reduction of Vmax and action potential shortening were frequency dependent: the former was more prominent at shorter, while the latter at longer pacing cycle lengths. A rate dependent Vmax block, having rapid offset kinetics [{tau} = 91 (20) ms], was observed in addition to tonic block. Under voltage clamp conditions, a variety of ion currents were blocked by articaine: ICa [EC50 = 471 (75) µM], Ito [EC50 = 365 (62) µM], IK1 [EC50 = 372 (46) µM], IKr [EC50 = 278 (79) µM], and IKs [EC50 = 326 (65) µM]. Hill coefficients were close to unity indicating a single binding site for articaine, except for IK1.

Conclusions: Articaine can modify cardiac action potentials and ion currents at concentrations higher than the therapeutic range which can be achieved only by accidental venous injection. Since its suppressive effects on the inward and outward currents are relatively well balanced, the articaine-induced changes in action potential morphology may be moderate even in the case of overdose.

Keywords: anaesthetics, local; ions, ion channels; heart; pharmacology


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