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Turku PET Centre, Centre for Cognitive Neuroscience, and the Department of Pharmacology and Clinical Pharmacology, University of Turku, and the Departments of Anesthesiology and Intensive Care, Child Neurology, and Psychiatry, Turku University Hospital, Turku, Finland; Institute of Biomedicine, Pharmacology, University of Helsinki, Helsinki, Finland
Address correspondence to Elina Salmi, MD, Turku PET Centre, PO Box 52, FIN-20521 Turku, Finland. Address e-mail to anelsa{at}utu.fi.
Positron emission tomography (PET) studies suggest that propofol and inhaled anesthetics increase 11C-flumazenil binding in the living human brain, thus supporting the involvement of
-aminobutyric acid type A (GABAA) 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 GABAA receptor agonistic properties. By using PET, we studied the cerebral 11C-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 11C-flumazenil binding to GABAA receptor in the brain, indicating that this mechanism is of minor importance in the actions of subanesthetic ketamine.
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