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- W2021796111 abstract "In Brief Drugs that block N-methyl-d-aspartate glutamate receptors or that promote γ-aminobutyric acid type A inhibition trigger neuroapoptosis in the developing rodent brain. Propofol reportedly interacts with both γ-aminobutyric acid type A and N-methyl-d-aspartate glutamate receptors, but has not been adequately evaluated for its ability to induce developmental neuroapoptosis. Here we determined that the intraperitoneal (i.p.) dose of propofol required to induce a surgical plane of anesthesia in the infant mouse is 200 mg/kg. We then administered graduated doses of propofol (25–300 mg/kg i.p.) and found that doses ≥50 mg/kg induce a significant neuroapoptosis response. We conclude that propofol induces neuroapoptosis at 1/4 the dose required for surgical anesthesia. IMPLICATIONS: Propofol is used for sedation and anesthesia in pediatric and obstetric medicine. Subanesthetic exposure of infant mice to other anesthetics (ketamine, midazolam, and isoflurane) triggers neuroapoptosis in the developing brain. We now report that propofol, in subanesthetic doses, triggers neuroapoptosis in the infant mouse brain." @default.
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- W2021796111 date "2008-06-01" @default.
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- W2021796111 title "Subanesthetic Doses of Propofol Induce Neuroapoptosis in the Infant Mouse Brain" @default.
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- W2021796111 doi "https://doi.org/10.1213/ane.0b013e318172ba0a" @default.
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