Correspondence  |   February 2017
Flumazenil Modulation of the γ-Aminobutyric Acid Type A Receptor: Competitive versus Noncompetitive Antagonism at the Agonist-binding Site
Author Notes
  • Massachusetts General Hospital, Boston, Massachusetts. draines@partners.org
  • (Accepted for publication October 11, 2016.)
    (Accepted for publication October 11, 2016.)×
Article Information
Correspondence
Correspondence   |   February 2017
Flumazenil Modulation of the γ-Aminobutyric Acid Type A Receptor: Competitive versus Noncompetitive Antagonism at the Agonist-binding Site
Anesthesiology 2 2017, Vol.126, 350-351. doi:10.1097/ALN.0000000000001444
Anesthesiology 2 2017, Vol.126, 350-351. doi:10.1097/ALN.0000000000001444
A variety of therapeutic drugs administered by anesthesiologists are commonly and effectively pharmacologically reversed. Unfortunately, and somewhat ironically, general anesthetics are not among them. It was, therefore, with great interest that I read the article “Effects of γ-Aminobutyric Acid Type A Receptor Modulation by Flumazenil on Emergence from General Anesthesia.1  Among the many interesting findings, this study demonstrated that flumazenil can reduce isoflurane-mediated potentiation of the γ-aminobutyric acid (GABA) type A receptor (GABAAR) in the presence of GABA, weakly activate GABAARs in the absence of GABA, and shorten the time required for the electroencephalogram to return to an awake-like state after isoflurane administration.
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