Correspondence  |   February 2017
In Reply
Author Notes
  • Emory University, Atlanta, Georgia (P.S.G.). pgarcia@emory.edu
  • (Accepted for publication October 11, 2016.)
    (Accepted for publication October 11, 2016.)×
Article Information
Correspondence
Correspondence   |   February 2017
In Reply
Anesthesiology 2 2017, Vol.126, 352-353. doi:10.1097/ALN.0000000000001446
Anesthesiology 2 2017, Vol.126, 352-353. doi:10.1097/ALN.0000000000001446
We thank Dr. Raines for his interest in our work and thoughtful comments on the molecular pharmacology underlying our observed effects.
Our study1  was primarily motivated by commonly encountered clinical scenarios, and our conclusions focused on network and in vivo actions of the combination of flumazenil in the setting of decreasing isoflurane concentration. While we are confident in concluding that flumazenil modulates emergence in rodents, there are insufficient data to completely describe the range of pharmacologic interactions between flumazenil and γ-aminobutyric acid (GABA) type A receptors (GABAARs), including site-specific interactions. Our demonstration of “antagonistic activity” by flumazenil on GABAARs in heterologous expression systems in the presence and absence of coapplied isoflurane mainly served to emphasize a GABA-mediated effect of flumazenil and isoflurane.
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