Siegers C P, Biltz H, Wächter S
Anaesthesist. 1979 Aug;28(8):373-7.
Rats exposed to halothane (100 ppm) in a closed allglass-system eliminate halothane from the atmosphere of this system with a half-life (t0.5) of 0.99 h. In 24 h-fasted rats t0.5 was prolonged to 1.24 h. A single oral load of 4.8 g/kg ethanol as well as a 15% ethanol solution instead of drinking water for 28 days did not alter the metabolic elimination of halothane. On the other hand, ethanol (4.8 g/kg p.o.) applied 5 min before exposure to halothane markedly prolonged t0.5 to 3.79 h. Pretreatment with phenobarbital (80 mg/kg i.p. for 4 days) shortened t0.5 significantly to 0.79 h. Inhibition of the mixed-function oxidase system by dithiocarb (100 mg/kg i.p.) or diethyl maleate (1 ml/kg i.p.) markedly prolonged t0.5 to 7.53 and 1.57 h. respectively. The observed modifications of the halothane metabolism may be of interest in relation to the problem of halothane-induced hepatotoxicity.
在封闭的全玻璃系统中暴露于氟烷（100 ppm）的大鼠，将该系统空气中的氟烷清除，其半衰期（t0.5）为0.99小时。禁食24小时的大鼠t0.5延长至1.24小时。单次口服4.8 g/kg乙醇以及用15%乙醇溶液代替饮用水持续28天，并未改变氟烷的代谢清除。另一方面，在暴露于氟烷前5分钟口服乙醇（4.8 g/kg）显著将t0.5延长至3.79小时。用苯巴比妥（80 mg/kg腹腔注射，持续4天）预处理可将t0.5显著缩短至0.79小时。二硫代氨基甲酸盐（100 mg/kg腹腔注射）或马来酸二乙酯（1 ml/kg腹腔注射）对混合功能氧化酶系统的抑制分别显著将t0.5延长至7.53小时和1.57小时。观察到的氟烷代谢改变可能与氟烷诱导的肝毒性问题有关。
