Effects of ethanol on rat brain and heart acetylcholine.

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Abstract
Single doses of ethanol (6 g/kg of body weight in a 50% vol/vol solution) were administered by stomach tube to male Sprague-Dawley rats which were either permitted laboratory chow and water ad lib until sacrifice (fed rats) or were fasted 17 h prior to intubation. Control animals received equal volumes of saline or isocaloric glucose or no intubation. The animals were sacrificed at various intervals after intubation and immediately thereafter the brains and hearts were excised and acetylcholine (ACh) was extracted and analyzed by a pyrolysis-gas chromatographic method. The identity of the compound analyzed as ACh was confirmed by mass spectrometry. Fasting alone caused a reduction in brain ACh levels: the mean level in fed rats was 26.0 nmol/g; in fasted animals, 22.8. Ethanol caused increases in brain ACh in fed and fasted rats. The mean brain ACh in 6 fed ethanol-treated rats was 32.5 nmol/g 2 h after intubation; in 18 untreated fed controls it was 26.0. In the ethanol-treated rats, brain ACh returned to control values at 4.5 h. In 6 fasted ethanol-treated rats the maximum effect of ethanol on brain ACh was seen 4 h after intubation: 31.2 nmol/g vs. 22.8 in 18 untreated fasted controls. No changes in brain ACh were found in glucose or saline treated animals. No differences were found between heart ACh concentrations in fed and fasted controls and no changes in heart ACh occurred after ethanol, saline or glucose administration in either group. Increased brain ACh levels may be associated with the general depressant effect of ethanol on the CNS.

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