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BJA Advance Access originally published online on July 1, 2005
British Journal of Anaesthesia 2005 95(3):305-309; doi:10.1093/bja/aei185
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© The Board of Management and Trustees of the British Journal of Anaesthesia 2005. All rights reserved. For Permissions, please e-mail: journal.permissions@oupjournals.org

Halothane and sevoflurane inhibit Na/Ca exchange current in rat ventricular myocytes

G. Bru-Mercier1, P. M. Hopkins2 and S. M. Harrison1,*

1 School of Biomedical Sciences and 2 Academic Unit of Anaesthesia, University of Leeds, Leeds LS2 9JT, UK

* Corresponding author. E-mail: s.m.harrison{at}leeds.ac.uk

Background. The electrogenic Na+/Ca2+ exchanger (NCX) represents the main extrusion pathway for Ca2+ in ventricular muscle and therefore plays an important role in the regulation of cytosolic Ca2+ and contraction. Halothane and sevoflurane modulate cytosolic Ca2+ regulation and at steady state are negatively inotropic, however, the involvement of anaesthetic-induced changes in NCX activity in these effects requires further study.

Methods. Ventricular myocytes were isolated using a standard collagenase/protease dispersion technique and superfused with a physiological salt solution at 30°C. Whole-cell patch-clamp technique was used to control membrane voltage. INCX (identified as Ni2+ sensitive current) was recorded using a ramp clamp protocol under conditions to inhibit contaminating currents.

Results. With 0.6 mM sevoflurane, outward INCX at positive voltages (≥0 mV) and inward INCX at voltages negative to –60 mV was significantly reduced (P<0.05, n=13; INCX reduced by 48% at +50 and 65% of control at –120 mV). Halothane (0.6 mM) inhibited outward INCX at voltages positive to –10 mV and inward INCX at voltages negative to –80 mV (P<0.05, n=10; INCX reduced by 64% at +50 and 65% of control at –120 mV). Anaesthetic-induced inhibition of both inward and outward current was not voltage-dependent.

Conclusions. Inhibition of Ca2+ efflux via NCX (i.e. inward INCX) during an exposure to halothane or sevoflurane would be expected to limit the negative inotropic effects of these agents and help maintain SR Ca2+ content.


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