Demonstration of halothane-induced hepatic lipid peroxidation in rats by quantification of F2-isoprostanes.
Demonstration of halothane-induced hepatic lipid peroxidation in rats by quantification of F2-isoprostanes.
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通过定量 F2-异前列腺素证明氟烷诱导的大鼠肝脂质过氧化。
DOI：
10.1097/00000542-199604000-00019
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发表时间：
1996
期刊：
影响因子：
8.8
通讯作者：
Franks,JJ
中科院分区：
文献类型：
--
作者：
Awad,JA;Horn,JL;Roberts2nd,LJ;Franks,JJ
背景氟烷可以还原代谢为可能引发脂质过氧化的自由基中间体。 Sprague-Dawley 大鼠缺氧和苯巴比妥预处理可增加氟烷的还原代谢。 F (2)-异前列腺素是体内脂质过氧化的一种新测量方法，用于量化氟烷诱导的大鼠脂质过氧化。方法将大鼠暴露于 1% 氟烷或 14% O (2) 中 2 小时。预处理包括苯巴比妥、异烟肼或媒介物。大鼠还暴露于浓度为 21% O 的氟烷、安氟烷和地氟烷 (2)。通过 F (2)-异前列烷的质谱定量评估脂质过氧化。结果将苯巴比妥预处理的大鼠暴露于 21% O (2) 的 1% 氟烷中 2 小时，导致肝脏和血浆 F (2)-异前列烷浓度比非氟烷对照大鼠增加五倍。 14% O (2) 会增强氟烷诱导的增加，但单独缺氧没有显着效果。仅 1% 氟烷/14% O (2) 组 24 小时时的丙氨酸转氨酶活性显着增加。通过比较低氧条件下异烟肼和苯巴比妥预处理与不预处理的效果，确定细胞色素 P450 酶诱导对氟烷诱导的 F(2)-异前列烷产生和肝损伤的影响。在未经预处理的大鼠中，氟烷引起血浆和肝脏 F (2)-异前列腺素分别增加 4 倍和 11 倍，而异烟肼预处理则没有效果。苯巴比妥预处理可增强氟烷诱导的脂质过氧化，血浆和肝脏中的 F (2)-异前列腺素分别增加 9 倍和 20 倍。丙氨酸转氨酶活性仅在该组中增加。在环境氧浓度下，氟烷而非安氟烷或地氟烷会导致 F (2)-异前列腺素增加。 结论 通过定量 F (2)-异前列腺素，在 Sprague-Dawley 大鼠中证实了特异性氟烷诱导的脂质过氧化作用，并且通过缺氧和苯巴比妥预处理而增加，但异烟肼预处理不会增加。
BackgroundHalothane can be reductively metabolized to free radical intermediates that may initiate lipid peroxidation. Hypoxia and phenobarbital pretreatment in Sprague-Dawley rats increases reductive metabolism of halothane. F (2)-isoprostanes, a novel measure of lipid peroxidation in vivo, were used to quantify halothane-induced lipid peroxidation in rats.MethodsRats were exposed to 1% halothane or 14% O (2) for 2 h. Pretreatments included phenobarbital, isoniazid, or vehicle. Rats also were exposed to halothane, enflurane, and desflurane at 21% O (2). Lipid peroxidation was assessed by mass spectrometric quantification of F (2)-isoprostanes.ResultsExposure of phenobarbital-pretreated rats to 1% halothane at 21% O (2) for 2 h caused liver and plasma F (2)-isoprostane concentrations to increase fivefold compared to nonhalothane control rats. This halothane-induced increase was enhanced by 14% O (2), but hypoxia alone had no significant effect. Alanine aminotransferase activity at 24 h was significantly increased only in the 1% halothane/14% O (2) group. The effect of cytochrome P450 enzyme induction on halothane-induced F (2)-isoprostane production and liver injury was determined by comparing the effects of isoniazid and phenobarbital pretreatment with no pretreatment under hypoxic conditions. Halothane caused 4-and 11-fold increases in plasma and liver F (2)-isoprostanes, respectively, in non-pretreated rats, whereas isoniazid pretreatment had no effect. Phenobarbital pretreatment potentiated halothane-induced lipid peroxidation with 9-and 20-fold increases in plasma and liver F (2)-isoprostanes, respectively. Alanine aminotransferase activity was increased only in this group. At ambient oxygen concentrations, halothane but not enflurane or desflurane, caused F (2)-isoprostanes to increase.ConclusionsSpecific halothane-induced lipid peroxidation was demonstrated in Sprague-Dawley rats using quantification of F (2)-isoprostanes and was increased by hypoxia and phenobarbital pretreatment, but not isoniazid pretreatment.
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酸中毒对交感肾上腺刺激的影响。
DOI：
--
发表时间：
1966
期刊：
Journal of the American Medical Association (JAMA)
影响因子：
--
作者：
J. Malm;W. Manger;S. F. Sullivan;E. M. Papper;G. Nahas
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影响因子：
8.8
作者：
J. Sharp;J. Trudell;E. N. Cohen
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E. N. Cohen
影响因子：
4.1
作者：
H. Hughes;I. M. George;J. Evans;C. Rowlands;G. Powell;C. Curtis
通讯作者：
C. Curtis
影响因子：
2.9
作者：
MORROW, JD;HARRIS, TM;ROBERTS, LJ
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ROBERTS, LJ
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DOI：
--
发表时间：
1971
期刊：
影响因子：
--
作者：
J. Bunker
通讯作者：
J. Bunker