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 À1 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 À1 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 À1 i.p. propofol was not significantly different between ethanoltreated 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.
We experienced a case of a huge hemangioma occupying the oropharyngeal space in an 11-year-old child. Although urgent surgical tracheostomy under local anesthesia was suggested initially, medical interview and findings of computerized tomography and fiberoptic laryngoscopy revealed that the airway of the patient was relatively stable when she was in the semi-left decubitus position. General anesthetic induction would have had potential risks of airway obstruction. Thus, after placing the patient in the semi-left decubutus position, we chose semi-awake induction to secure the airway. With a small dose of fentanyl, we accomplished orotracheal intubation. In this report, we discuss the importance of referring to an airway management algorithm when encountering a difficult airway.
Our results demonstrated that R(-)-MPPB decreased, while S(+)-MPPB increased, rat hippocampal ACh release and that the inhibitory effects of R(-)-MPPB may involve the GABA(A) receptor in vivo. These data imply that changes in hippocampal ACh due to these agents may be related to their central inhibitory and stimulatory actions in vivo.
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