British Journal of Anaesthesia, Vol 82, Issue 3 402-411, Copyright © 1999 by The Board of Management and Trustees of the British Journal of Anaesthesia
K. Kameyama, K. Aono and K. Kitamura
To help clarify the mechanisms by which volatile anaesthetics act on
neuronal Ca2+ channel currents (IBa), the effects of isoflurane were
studied on IBa in rat dorsal root ganglion (DRG) cells. Voltage- dependent
IBa were pharmacologically subdivided into L-, N- and P/Q- types, and
toxin-resistant IBa. At clinically relevant concentrations, isoflurane
inhibited the L-, N- and P/Q-types, but not toxin-resistant IBa. The IC50
values for the L-, N- and P/Q-types were 0.7%, 1.3% and 3.0%, respectively
(concentrations equivalent to 0.35, 0.68 and 1.46 mmol litre-1 in the
aqueous phase). Isoflurane also produced initial transient augmentation of
the N-type IBa. Isoflurane shifted the mid- point of the steady-state
inactivation curve for the L-, N- and P/Q- type IBa towards negative
potentials, and prolonged the time constant of current reactivation. We
conclude that isoflurane inhibited L-, N- and P/Q-type IBa in rat DRG
neurones by enhancing current inactivation and prolonging recovery time
after inactivation. Transient augmentation of the N-type IBa may also form
part of the overall actions of isoflurane in DRG neurones.
LABORATORY INVESTIGATIONS
Isoflurane inhibits neuronal Ca2+ channels through enhancement of current inactivation
Department of Anaesthesiology and Department of Pharmacology, Fukuoka Dental College, 2-15-1 Tamura, Sawara-ku, Fukuoka 814-0193, Japan
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