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• W2075879574 abstract "Central nervous system oxygen toxicity (CNS-OT) seizures occur with little or no warning, and no effective mitigation strategy has been identified. Ketogenic diets (KD) elevate blood ketones and have successfully treated drug-resistant epilepsy. We hypothesized that a ketone ester given orally as R, S-1,3-butanediol acetoacetate diester (BD-AcAc 2 ) would delay CNS-OT seizures in rats breathing hyperbaric oxygen (HBO 2 ). Adult male rats ( n = 60) were implanted with radiotelemetry units to measure electroencephalogram (EEG). One week postsurgery, rats were administered a single oral dose of BD-AcAc 2 , 1,3-butanediol (BD), or water 30 min before being placed into a hyperbaric chamber and pressurized to 5 atmospheres absolute (ATA) O 2 . Latency to seizure (LS) was measured from the time maximum pressure was reached until the onset of increased EEG activity and tonic-clonic contractions. Blood was drawn at room pressure from an arterial catheter in an additional 18 animals that were administered the same compounds, and levels of glucose, pH, Po 2 , Pco 2 , β-hydroxybutyrate (BHB), acetoacetate (AcAc), and acetone were analyzed. BD-AcAc 2 caused a rapid (30 min) and sustained (>4 h) elevation of BHB (>3 mM) and AcAc (>3 mM), which exceeded values reported with a KD or starvation. BD-AcAc 2 increased LS by 574 ± 116% compared with control (water) and was due to the effect of AcAc and acetone but not BHB. BD produced ketosis in rats by elevating BHB (>5 mM), but AcAc and acetone remained low or undetectable. BD did not increase LS. In conclusion, acute oral administration of BD-AcAc 2 produced sustained ketosis and significantly delayed CNS-OT seizures by elevating AcAc and acetone." @default.
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• W2075879574 date "2013-05-15" @default.
• W2075879574 modified "2023-10-18" @default.
• W2075879574 title "Therapeutic ketosis with ketone ester delays central nervous system oxygen toxicity seizures in rats" @default.
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• W2075879574 doi "https://doi.org/10.1152/ajpregu.00506.2012" @default.
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