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在給予小鼠安他布斯(120毫克/公斤,口服)2小时后,戊巴比妥鈉睡眠时間显著延长,同时肝糖元含量下降;24小时后作用消失。由于本药能延緩戊巴比妥鈉自小鼠体內消失而不改变維持动物睡眠所必須的最低催眠药水平,可見安他布斯这种“延长”效应是因为抑制了催眠药的生物轉化,而并非通过中樞协同机制。安他布斯并不改变小鼠戊巴比妥鈉的ED_(50)及二乙基巴比妥(一个在体內不經轉化的催眠药)睡眠时間,也支持这个論断。大鼠体外肝切片試驗表明,当安他布斯濃度为6.6×10~(-5)M时即抑制戊巴比妥鈉轉化的50％。安他布斯对药酶的抑制作用属于竞爭性,谷胱甘肽、半胱氨酸及維生素C不能对抗此作用。安他布斯对氯丙嗪的氧化影响不大,对对硝基苯甲酸的还原无抑制作用。
After 2 hours’ administration of amphetamines (120 mg / kg orally) to mice, the sleep time of pentobarbital sodium was significantly prolonged, meanwhile, the content of hepatic glycogen was decreased; the action disappeared after 24 hours. As the drug can delay the disappearance of pentobarbital sodium from mice without changing the minimum hypnotic level necessary to maintain animal sleep, this “prolongation” effect of Anabus can be attributed to the inhibition of the biotransformation of hypnotics , Not through the central coordination mechanism. Anabesi also supports this statement by not modifying the mice sleep time with sodium pentobarbital ED 50 and diethylbarbituride, a hypnotic drug that is not converted in the body. In vitro rat liver sections showed that 50% of pentobarbital sodium was inhibited when the concentration of Anabuse was 6.6 × 10 ~ (-5) M. Antibacterial activity of Anabesuib is competitive, and glutathione, cysteine and vitamin C do not counteract this effect. Anabuse on the oxidation of chlorpromazine little effect on the reduction of p-nitrobenzoate no inhibitory effect.