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pubmed-article:1319600pubmed:abstractTextAcute alcohol administration to rats has in preliminary studies been reported to drastically increase the binding of the benzodiazepine (BZ) receptor antagonist [3H]flumazenil (Ro 15-1788) to central BZ receptors. In the present study the effect of acute alcohol ingestion on the disposition of [11C]flumazenil in the human brain and plasma was examined by positron emission tomography (PET) in four healthy volunteers. Neocortex, cerebellum and pons (reference region) were delineated using X-ray computerized tomography (CT). Alcohol did not increase either total radioactivity uptake or specific [11C]flumazenil binding in neocortex or cerebellum. However, alcohol had a small but significant effect on [11C]flumazenil in arterial blood. After alcohol the plasma radioactivity peak was higher, more narrow and occurred earlier than in the control experiments. The present experiments contradict the view that alcohol directly affects central BZ receptor binding in man. Thus the dramatic increase of flumazenil binding in rat brain reported previously could not be observed in the human brain.lld:pubmed
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pubmed-article:1319600pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:1319600pubmed:articleTitlePET analysis of alcohol interaction with the brain disposition of [11C]flumazenil.lld:pubmed
pubmed-article:1319600pubmed:affiliationDepartment of Psychiatry and Psychology, Karolinska Institute, Stockholm, Sweden.lld:pubmed
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pubmed-article:1319600pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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