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雄性ＳＤ大鼠饮用含苯巴比妥（１ｍｇ／ｍｌ）的饮水一周后，随机分为６组，每组６例：ＮＣ，２１％Ｏ２／７９％Ｎ２；ＨＣ，１４％０；１８６％Ｎｅ；ＮＨ，２１％Ｏ２／７９％Ｎ２／１．２ＭＡＣ氟烷；ＨＨ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ氟烷；ＮＳ，２１％Ｏ２／７９％Ｎ２／１．２ＭＡＣ七氟醚；ＨＳ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ七氟醚。吸入时间１ｈ，２４ｈ后测定血浆及肝匀浆中ＭＤＡ、ＳＯＤ、游离琉基的含量。结果ＨＨ、ＮＨ组肝匀浆及血浆中ＭＤＡ、ＳＯＤ的含量均高于其它各组（Ｐ＜０．０１，Ｐ＜０．０５），余各组间均无显著差异（Ｐ＞０．０５）。ＮＨ、ＨＨ组血浆及肝匀浆中游离琉基的含量显著低于其它各组（Ｐ＜０．０１）。提示氟烷所致的肝脂过氧化反应增强的作用可能与其肝毒性有关，而七氟醚无促进肝脏脂过氧化反应增强的作用。
One week after drinking water containing phenobarbital (1 mg / ml), male Sprague-Dawley rats were randomly divided into 6 groups with 6 rats in each group: NC, 21% O2 / 79% N2; HC, 14% HN, 14% O2 / 86% N2 / 1.2 MAC HFC; NS, 21% O2 / 79% N2 / 1.2 MAC sevoflurane; HS, 14% O2 / 86% N2 / 1.2 MAC sevoflurane. Inhalation time 1h, 24h after the determination of plasma and liver homogenate MDA, SOD, free radical content. Results The contents of MDA and SOD in the liver homogenates and plasma of HH and NH groups were higher than those in other groups (P <0.01, P <0.05), but there were no significant differences among the other groups (P> 0.05 ). The contents of free primidin in plasma and liver homogenate of NH, HH group were significantly lower than those of other groups (P <0.01). Tip HFA-induced hepatic lipid peroxidation increased role may be related to its hepatotoxicity, and sevoflurane did not promote liver lipid peroxidation enhanced role.