Adenosine involves in delayed recovery from sedation/hypnosis

2016 Fiscal Year Final Research Report

• Project/Area Number: 26463079
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Surgical dentistry
• Research Institution: Asahi University
• Principal Investigator: Sakurai Satoru 朝日大学, 歯学部, 教授 (50225843)
• Co-Investigator(Renkei-kenkyūsha): GOTO TAKASHI 朝日大学, 歯学部, 講師 (30637898)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: アデノシン / アミノフィリン / ミダゾラム

Outline of Final Research Achievements

Flumazenil, a specific benzodiazepine antagonist that acts on GABA receptors via competitive inhibition, initially caused rapid and complete antagonism and all subjects seemingly fully awake responding properly in response to verbal command. However, flumazenil administration resulted in high incidence of resedation, particularly when higher dose was given.
Midazolam and flumazenil potently inhibit adenosine uptake, thereby accumulating extracellular concentration of adenosine, and thus potentiate actions of adenosine. Adenosine excites a subset of sleep-promoting neurons.
In this study, because aminophylline antagonised the resedation that occurred after flumazenil administration, adenosine may be associated with this resedation. Aminophylline, a nonselective adenosine receptor antagonist, has been shown to be an effective agent in reversing the sedative effects of midazolam, because midazolam and flumazenil enhances extracellular adenosine levels in the cerebral cortex.

Free Research Field

歯科麻酔