Morio M, Fujii K, Satoh N, Imai M, Kawakami U, Mizuno T, Kawai Y, Ogasawara Y, Tamura T, Negishi A
Hiroshima University, Japan.
Anesthesiology. 1992 Dec;77(6):1155-64. doi: 10.1097/00000542-199212000-00017.
Sevoflurane previously has been reported to undergo extensive degradation in the presence of soda lime. To more completely characterize the extent and significnce of this reaction, we studied degradation of sevoflurane with and without soda lime, as well as the toxicity and mutagenicity of the degradation products. Two degradation products detected were CF2 = C(CF3)OCH2F (compound A) and CH3OCF2CH(CF3)OCH2F (compound B). During circulation of 1%, 2%, and 3% sevoflurance in a closed anesthesia circuit for 8 h, peak concentrations of compound A were 13.3 +/- 0.27, 30.2 +/- 0.10, and 42.1 +/- 1.07 ppm at 2 h, respectively. The concentrations of compound B did not exceed 2 ppm. The temperature of the soda lime was 43.3 +/- 2.8 degrees C at 1 h and increased gradually to 47.9 +/- 1.5 degrees C after 8 h. In closed flasks with soda lime, the magnitude of the decrease in sevoflurance concentrations (3%) and of the increase in compound A concentrations was temperature dependent. The peak concentrations of compound A at 23 degrees C, 37 degrees C, and 54 degrees C were 32.8 +/- 6.8 at 2 h, 46.6 +/- 1.0 at 0.5 h, and 78.5 +/- 2.3 ppm at 0.5 h, respectively. The LC50 (50% lethal concentration) of compound A in Wistar rats was 1,090 ppm in males and 1,050 ppm in females exposed for 1 h. The LC50 was 420 ppm in males and 400 ppm in females exposed for 3 h. The chronic toxicity of compound A in Wistar rats was studied by exposing rats 24 times, for 3 h each, to initial concentrations of 30, 60, or 120 ppm in a ventilated chamber. At all concentrations, there were no apparent effects other than a loss of body weight in females (120 ppm) on the final day (P < 0.01). Compound A did not induce mutation on the reverse (Ames) test at less than 2,500 micrograms/dish (culture medium 2.7 ml) with activation by S-9 mixture, and below 1,250 micrograms/dish (culture medium 2.7 ml) without activation, in four strains of S. typhimurium and in 1 strain of E. coli. Exposure of fibroblasts to 7,500 ppm of compound A for 1 h, compound A did not induce structural change. In a study of acute toxicity of compound B, there was no toxicity in Wistar rats after 3 h of exposure at 2,400 ppm. The reverse (Ames) test for compound B was negative at 625-1,250 micrograms/dish.(ABSTRACT TRUNCATED AT 400 WORDS)
先前有报道称,七氟醚在碱石灰存在的情况下会发生大量降解。为了更全面地描述该反应的程度和意义,我们研究了有碱石灰和无碱石灰时七氟醚的降解情况,以及降解产物的毒性和致突变性。检测到的两种降解产物分别是CF2 = C(CF3)OCH2F(化合物A)和CH3OCF2CH(CF3)OCH2F(化合物B)。在封闭的麻醉回路中,1%、2%和3%的七氟醚循环8小时,化合物A在2小时时的峰值浓度分别为13.3±0.27、30.2±0.10和42.1±1.07 ppm。化合物B的浓度未超过2 ppm。碱石灰在1小时时的温度为43.3±2.8℃,8小时后逐渐升至47.9±1.5℃。在装有碱石灰的封闭烧瓶中,七氟醚浓度降低(3%)的幅度和化合物A浓度增加的幅度与温度有关。在23℃、37℃和54℃时,化合物A在2小时时的峰值浓度分别为32.8±6.8 ppm、在0.5小时时为46.6±1.0 ppm、在0.5小时时为78.5±2.3 ppm。在Wistar大鼠中,化合物A暴露1小时的半数致死浓度(LC50),雄性为1090 ppm,雌性为1050 ppm。暴露3小时时,雄性为420 ppm,雌性为400 ppm。通过在通风箱中对大鼠进行24次每次3小时的暴露,研究了化合物A对Wistar大鼠的慢性毒性,初始浓度为30、60或120 ppm。在所有浓度下,除了最后一天雌性(120 ppm)体重减轻外(P<0.01),没有明显影响。在有S-9混合物激活的情况下,化合物A在每皿低于2500微克(培养基2.7毫升)、无激活时低于1250微克(培养基2.7毫升)的情况下,对四株鼠伤寒沙门氏菌和一株大肠杆菌进行回复(艾姆斯)试验时,未诱导突变。将成纤维细胞暴露于7500 ppm的化合物A 1小时,化合物A未诱导结构变化。在化合物B的急性毒性研究中,Wistar大鼠暴露于2400 ppm 3小时后没有毒性。化合物B的回复(艾姆斯)试验在625 - 1250微克/皿时为阴性。(摘要截短于400字)