Subanesthetic ketamine does not affect 11C-flumazenil binding in humans.

Positron emission tomography (PET) studies suggest that propofol and inhaled anesthetics increase (11)C-flumazenil binding in the living human brain, thus supporting the involvement of gamma-aminobutyric acid type A (GABA(A)) receptors in the mechanism of action of these drugs. Ketamine produces its anesthetic effects primarily by N-methyl-d-aspartate receptor antagonism, but it may also have GABA(A) receptor agonistic properties. By using PET, we studied the cerebral (11)C-flumazenil binding in 10 healthy subjects before and during a subanesthetic racemic ketamine infusion reaching a serum concentration of 350 +/- 42 ng/mL. Ketamine did not affect (11)C-flumazenil binding to GABA(A) receptor in the brain, indicating that this mechanism is of minor importance in the actions of subanesthetic ketamine.