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BJA Advance Access published online on December 23, 2005
British Journal of Anaesthesia, doi:10.1093/bja/aei309
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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: journals.permissions@oxfordjournals.org
Accepted November 21, 2005

Laboratory Investigation

Nitrous oxide depresses electroencephalographic responses to repetitive noxious stimulation in the rat

M. L. LeDuc 1, R. Atherley 1, S. L. Jinks 1, and J. F. Antognini 2 *

1 Department of Anesthesiology and Pain Medicine, University of California, Davis, CA, USA
2 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. Although N2O has been widely used as an anaesthetic adjuvant its effect on electroencephalographic (EEG) activity is poorly understood because it is usually studied in the presence of additional anaesthetics, including inhaled anaesthetics. We examined the EEG effects of N2O in rats using a hyperbaric chamber that permitted N2O to be the sole anaesthetic.

Methods. Rats (n=10) were anaesthetized with isoflurane and EEG activity was recorded from skull screws. The rats were placed into a hyperbaric chamber and mechanically ventilated. Isoflurane was eliminated while the chamber was pressurized with N2O. The minimum alveolar concentration (MAC) was determined in five rats by adjusting the chamber pressure and N2O concentration, and applying a tetanic noxious stimulus to the tail via an electrical pass-through. EEG responses to noxious stimulation (20 electrical pulses at 40 V applied to the tail at 0.1, 1 and 3 Hz, and 50 Hz tetanic stimulation at 60 mA applied for 30 s) were determined at 1.5 and 2 atm N2O.

Results. The N2O MAC was 1.7±0.1 atm. No consistent EEG activation occurred during electrical stimulation at either partial pressure of N2O, although spontaneous EEG activation often occurred. Blood pressure increased after the 3 and 50 Hz stimuli. Four other rats anaesthetized with isoflurane had EEG activation with the 3 and 50 Hz stimuli.

Conclusions. These data indicate that N2O at peri-MAC partial pressures prevents EEG activation resulting from noxious electrical stimulation. Unlike the situation with isoflurane, stimulus-evoked EEG activation did not occur at peri-MAC anaesthetic concentrations, suggesting that N2O potently blocked ascending nociceptive transmission.

Keywords: anaesthesia; anaesthetics gases, nitrous oxide; monitoring, electroencephalography.
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