British Journal of Anaesthesia, Vol 79, Issue 1 78-83, Copyright © 1997 by The Board of Management and Trustees of the British Journal of Anaesthesia
R. Atcheson, K. Bjornstrom, R. A. Hirst, D. J. Rowbotham and D. G. Lambert
We have examined the effects of the volatile general anaesthetic agent,
halothane, on K+ and carbachol stimulated [3H]noradrenaline release and
associated increases in intracellular Ca2+ in a cultured human
neuroblastoma cell line, SH-SY5Y. K+ (but not carbachol) stimulated
[3H]noradrenaline release, and the increase in intracellular Ca2+
concentration was entirely extracellular Ca2+ dependent. Halothane produced
a dose-dependent reduction in K+ evoked release of [3H]noradrenaline with
significant inhibition (17%) occurring from 1.26 atm%. Basal and carbachol
evoked release were unaffected. Halothane also produced a dose-dependent
reduction in K+ evoked increases (measured at the peak) in intracellular
Ca2+ with significant inhibition (29%) occurring from 0.88 atm%. K+
plateau, basal and carbachol evoked increases in intracellular Ca2+ were
unaffected. These data suggest that halothane reduced Ca2+ entry through
voltage- sensitive Ca2+ channels and implicate this important class of ion
channel in the mechanism of anaesthesia.
LABORATORY INVESTIGATIONS
Effect of halothane on K+ and carbachol stimulated [3H]noradrenaline release and increased [Ca2+]i in SH-SY5Y human neuroblastoma cells
University Department of Anaesthesia, Leicester Royal Infirmary, Leicester LE1 5WW; Department of Anaesthesia and Intensive Care, University Hospital, S-581 85 Linkoping, Sweden
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