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From the *Department of Anesthesiology, WA University School of Medicine, Saint Louis, Missouri;
Department of Surgery, University of Pisa, School of Medicine, Pisa, Italy; and
Department of Psychiatry, WA University School of Medicine, Saint Louis, Missouri.
Address correspondence and reprint requests to Dr. John W. Olney, MD, Department of Psychiatry, Washington University School of Medicine, 660 South Euclid, PO BOX 8134, St. Louis, MO 63110. Address e-mail to olneyj{at}wustl.edu.
Abstract
Drugs that block N-methyl-d-aspartate glutamate receptors or that promote
-aminobutyric acid type A inhibition trigger neuroapoptosis in the developing rodent brain. Propofol reportedly interacts with both
-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.
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F. X. McGowan Jr and P. J. Davis Anesthetic-Related Neurotoxicity in the Developing Infant: Of Mice, Rats, Monkeys and, Possibly, Humans Anesth. Analg., June 1, 2008; 106(6): 1599 - 1602. [Full Text] [PDF] |
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