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Cerebral hypoxia-oligemia was produced by lowering of the arterial PO2 to 30 mm Hg and by right common carotid artery occlusion in rats who were pretreated with intravenous Krebs' solution, gamma-hydroxybutyrate (GHB) (500 mg/kg) or gamma-butyrolactone (GBL) (300 mg/kg). At 0.5 h exposure the right cerebral hemisphere of animals receiving Krebs', GHB or GBL showed equivalent decreases of ATP and phosphocreatine and increase of ADP, AMP and lactate which indicated that these depressant drugs had no beneficial effect on the energy metabolism of the acutely hypoxic-oligemic brain. In a second series of rats in which Krebs' solution, GHB or GBL were administered to animals during the early recovery period from 0.5 h hypoxic-oligemic exposure, the brain metabolic patterns of the right hemisphere indicated that GHB retarded the restitution of energy phosphates and the oxidation of the accumulated lactate; whereas, GBL led to a delayed metabolic deterioration. It is concluded that GHB and GBL do not beneficially alter cerebral energy metabolism during acute hypoxia-oligemia and that their administration during restitution may result in metabolic alterations which suggest an unfavorable effect.

Effects of gamma-hydroxybutrate and gamma-butyrolactone on cerebral energy metabolism during exposure and recovery from hypoxemia-oligemia.