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BJA Advance Access originally published online on September 3, 2004
British Journal of Anaesthesia 2004 93(5):737-739; doi:10.1093/bja/aeh263
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© The Board of Management and Trustees of the British Journal of Anaesthesia 2004

SHORT COMMUNICATION

Chronic ethanol consumption does not affect action of propofol on rat hippocampal acetylcholine release in vivo

G. Inagawa*, K. Sato, T. Kikuchi, M. Nishihama, M. Shioda, Y. Koyama, Y. Yamada and T. Andoh

Department of Anesthesiology, Yokohama City University School of Medicine, 3–9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan

* Corresponding author. E-mail: inagawa{at}med.yokohama-cu.ac.jp

Background. The aim of this study was to examine ethanol-consumption-related changes in the effects of propofol on rat hippocampal acetylcholine (ACh) release.

Methods. Male Sprague–Dawley rats received a solution of ethanol (20% v/v) for 24 weeks while controls received tap water. The effects of propofol were examined by in vivo microdialysis, with ACh release from the hippocampal regions determined by high-performance liquid chromatography with electrochemical detection (HPLC–ECD).

Results. Propofol 50 mg kg–1 i.p. significantly decreased basal hippocampal ACh release in ethanol-treated and control rats by 50.4 (SEM 4.7)% and 38.3 (11.1)%, respectively. Propofol 100 mg kg–1 i.p. significantly decreased basal hippocampal ACh release in ethanol-treated and control rats by 67.5 (3.7)% and 55.9 (7.4)%, respectively. The reduction in hippocampal ACh release induced by 50 or 100 mg kg–1 i.p. propofol was not significantly different between ethanol-treated and control rats. There was no significant difference in the duration of sleep between the two groups.

Conclusions. These results demonstrate that chronic ethanol consumption does not augment the inhibitory actions of propofol on rat hippocampal ACh release. These findings appear to be inconsistent with the notion that chronic ethanol intake enhances the propofol-induced inhibition of the hippocampal cholinergic system and related mental dysfunction.


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