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BJA Advance Access published online on July 28, 2005
British Journal of Anaesthesia, doi:10.1093/bja/aei208
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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
Accepted May 31, 2005

Laboratory Investigation

Halothane and propofol differentially affect electroencephalographic responses to noxious stimulation

M. Orth 1, L. Barter 1, C. Dominguez 2, R. Atherley 1, E. Carstens 3, and J. F. Antognini 4*

1 Department of Anesthesiology and Pain Medicine, University of California, Davis, CA, USA
2 Department of Anesthesiology, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA
3 Section of Neurobiology, Physiology and Behavior, University of California, Davis, CA, USA
4 Department of Anesthesiology and Pain Medicine, University of California, Davis, CA, USA; Section of Neurobiology, Physiology and Behavior, University of California, Davis, CA, USA

* To whom correspondence should be addressed.
J. F. Antognini, E-mail: jfantognini{at}ucdavis.edu


  Abstract

Background. Anaesthetics blunt neuronal responses to noxious stimulation, including effects on electroencephalographic (EEG) responses. It is unclear how anaesthetics differ in their ability to modulate noxious stimulation-evoked EEG activation. We investigated the actions of propofol and halothane on EEG responses to noxious stimuli, including repetitive electrical C-fibre stimulation, which normally evokes neuronal wind-up.

Methods. Rats were anaesthetized with halothane (n=8) or propofol (n=8), at 0.8x or 1.2x the amount required to produce immobility in response to tail clamping [minimum alveolar concentration (MAC) for halothane and median effective dose (ED50) for propofol]. We recorded EEG responses to repetitive electrical stimulus trains (delivered to the tail at 0.1, 1 and 3 Hz) as well as supramaximal noxious tail stimulation (clamp; 50 Hz electrical stimulus, each for 30 s).

Results. Under halothane anaesthesia, noxious stimuli evoked an EEG activation response manifested by increased spectral edge frequency (SEF) and median edge frequency (MEF). At 0.8 MAC halothane, the tail clamp increased the MEF from {approx}6 to {approx}8.5 Hz, and the SEF from {approx}25.5 to {approx}27 Hz. At both 0.8 and 1.2 MAC halothane, similar patterns of EEG activation were observed with the 1 Hz, 3 Hz and tetanic stimulus trains, but not with 0.1 Hz stimulation, which does not evoke wind-up. Under propofol anaesthesia, noxious stimuli were generally ineffective in causing EEG activation. At 0.8 ED50 propofol, only the tail clamp and 1 Hz stimuli increased MEF ({approx}8 to {approx}10-10.5 Hz). At the higher propofol infusion rate (1.2 ED50) the repetitive electrical stimuli did not evoke an EEG response, but the tetanic stimulus and the tail clamp paradoxically decreased SEF (from {approx}23 to {approx}21.5 Hz).

Conclusions. Propofol has a more significant blunting effect on EEG responses to noxious stimulation compared with halothane.

Keywords: anaesthetics i.v., propofol; anaesthetics volatile, halothane; brain, electroencephalography; model, rat; pain, experimental.
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