Subanesthetic ketamine does not affect 11C-flumazenil binding in humans.
prospective_cohort · Level II
Where this comes from
- Record sourced from PubMed, PMID 16115981.
- Also identified by DOI 10.1213/01.ANE.0000156951.83242.8D.
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Abstract
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.
Medical subject headings
- Brain
- Excitatory Amino Acid Antagonists
- Flumazenil
- GABA Modulators
- Ketamine