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British Journal of Anaesthesia, Vol 82, Issue 3 435-438, Copyright © 1999 by The Board of Management and Trustees of the British Journal of Anaesthesia

SHORT COMMUNICATIONS

Effect of bupivacaine on ATP-dependent potassium channels in rat cardiomyocytes

A. Olschewski, H. Olschewski, M. E. Brau, G. Hempelmann, W. Vogel and B. V. Safronov
Department of Anaesthesiology and Intensive Care Medicine, Department of Internal Medicine and Department of Physiology, Justus-Liebig-University, D-35392 Giessen, Germany

Bupivacaine induces fatal arrhythmia when accidentally injected i.v. or overdosed, whereas lidocaine is used as an anti-arrhythmic agent. We have suggested recently that the anti-arrhythmic effect of lidocaine may be explained by suppression of ATP-sensitive potassium (KATP) channels. Therefore, it could be argued that different sensitivities of KATP channels to both drugs could be a reason for their different arrhythmic and anti-arrhythmic properties. In this study, we have investigated the direct action of bupivacaine on KATP channels in cardiomyocytes. The effects of bupivacaine on the cardiac KATP channel were investigated using the patch-clamp technique on enzymatically dissociated cardiomyocytes of adult rats. Bupivacaine was applied to the outer side of excised membrane patches using a multiple-barrel perfusion system. Concentration-response curves indicated that bupivacaine blocked the mean current of the KATP channels at a half- maximum inhibiting concentration (IC50) of 29 microgramsmol litre-1, similar to that reported for lidocaine (43 microgramsmol litre-1). Binding of bupivacaine influenced the gating of this channel, but did not reduce the conductance of the open channel. Bupivacaine and lidocaine were equipotent in blocking KATP channels. However, because of its excessive block of the sodium channel in the inactivated state, block of KATP channels by bupivacaine will only enhance its cardiotoxicity.
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