• Chiaki Nemoto, Masahiro Murakawa, Takahiro Hakozaki, Tuyoshi Imaizumi, Tuyoshi Isosu, and Shinju Obara.
• Department of Anesthesiology, Fukushima Medical University School of Medicine, Hikarigaoka-1, Fukushima, Fukushima, 960-1295, Japan, nemo@fmu.ac.jp.
• J Anesth. 2013 Oct 1;27(5):771-4.

AbstractAcetylcholine plays an important role as a neurotransmitter in the central nervous system with involvement in both sleep and arousal. Dexmedetomidine, midazolam, and propofol are widely used for sedation of patients in intensive care medicine. In this study, we have examined the effect of continuous administration of dexmedetomidine, midazolam, and propofol on acetylcholine release in the rat cerebral cortex, using an in vivo microdialysis technique. Following infusion of a control solution, male Wistar rats (n = 6/group) were administered dexmedetomidine at 0.3 μg/kg/min, midazolam at 20 mg/kg/h, or propofol at 50 mg/kg/h over a 2-h period. Using a brain microdialysis method, extracellular acetylcholine concentrations were measured up to 2 h after administration of each agent at 15-min intervals. In the midazolam group, acetylcholine levels were significantly reduced with midazolam infusion, remaining low even after the drug was stopped. In the propofol group, acetylcholine levels were significantly decreased during propofol infusion, but returned to control levels once the infusion was stopped. Dexmedetomidine administration decreased acetylcholine release, but this finding was not statistically significant. From this study, midazolam and propofol but not dexmedetomidine significantly suppressed acetylcholine release in the cerebral cortex at sedative doses. Even though the righting reflex recovered almost the same after the cessation of drug administration, midazolam suppressed acetylcholine release longer than propofol.

15 keywords...

hide…