Subanesthetic doses of propofol induce neuroapoptosis in the infant mouse brain
Subanesthetic doses of propofol induce neuroapoptosis in the infant mouse brain
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DOI：
10.1213/ane.0b013e318172ba0a
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发表时间：
2008-06-01
影响因子：
5.7
通讯作者：
Olney, John W.
中科院分区：
文献类型：
--
作者：
Cattano, Davide;Young, Chainllie;Olney, John W.
阻断n -甲基- d -天冬氨酸受体或促进γ -氨基丁酸A型抑制的药物可触发发育中的啮齿动物大脑中的神经细胞凋亡。据报道，异丙酚与γ -氨基丁酸A型和n -甲基- d -天冬氨酸谷氨酸受体相互作用，但尚未充分评估其诱导发育性神经细胞凋亡的能力。在这里，我们确定在幼鼠中诱导手术平面麻醉所需的异丙酚腹腔注射剂量为200mg /kg。然后，我们给药的异丙酚分级剂量（25-300 mg/kg i.p.），发现剂量>= 50 mg/kg诱导显著的神经凋亡反应。我们得出结论，异丙酚在手术麻醉所需剂量的1/4时诱导神经凋亡。
Drugs that block N-methyl-D-aspartate glutamate receptors or that promote,gamma-aminobutyric acid type A inhibition trigger neuroapoptosis in the developing rodent brain. Propofol reportedly interacts with both gamma-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.