Effect of enzyme induction on plasma lipids using antipyrine, phenobarbital, and rifampicin
Effect of enzyme induction on plasma lipids using antipyrine, phenobarbital, and rifampicin
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使用安替比林、苯巴比妥和利福平诱导酶对血脂的影响
DOI：
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发表时间：
1979
期刊：
影响因子：
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通讯作者：
E. Peheim
中科院分区：
文献类型：
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作者：
E. Ohnhaus;B. Kirchhof;E. Peheim
用安替比林、苯巴比妥和利福平诱导19名健康人肝微粒体酶系统，并观察其对血脂的影响。在每次研究之前和之后，测定安替比林消除、γ-谷氨酰转肽酶、D-葡萄糖二酸和6-β-羟基皮质醇，并估计血脂（包括脂蛋白电泳）。受试者每天接受1，200 mg安替比林、100 mg苯巴比妥、600 mg利福平或1，200 mg利福平，持续14天。安替比林诱导酶后，安替比林半衰期从11.8小时降至8.7小时，苯巴比妥从13.8小时降至8.9小时，利福平（600 mg）从11.7小时降至7.1小时，利福平（1，200 mg），从11.7至5.6小时;安替比林、苯巴比妥、利福平（600 mg）和利福平给药后，安替比林清除率分别增加30%、56%、59%和（1,200毫克），125%。各组尿液中D-葡糖二酸排泄量均显示出相同程度的升高趋势，而安替比林和苯巴比妥对γ-谷氨酰转肽酶值的影响相似，但利福平治疗后保持不变。所有组中，经17-羟基皮质类固醇校正的6-β-羟基皮质醇尿排泄量均增加。血浆胆固醇、甘油三酯和其他血浆脂质测定值无变化，脂质电泳无变化。所用药物诱导微粒体酶系统后，胆固醇和血浆甘油三酯的稳态血浆浓度未升高。
The liver microsomal enzyme system was induced by antipyrine, phenobarbital, or rifampicin in 19 healthy subjects and the effect on plasma lipids was followed. Before and after each study antipyrine elimination, γ‐glutamyl‐transpeptidase, D‐glucaric acid, and 6‐β‐hydroxycortisol were measured, and plasma lipids including lipoprotein electrophoresis were estimated. The subjects were given 1,200 mg antipyrine, 100 mg phenobarbital, 600 mg rifampicin, or 1,200 mg rifampicin daily for 14 days. Following enzyme induction by antipyrine, the antipyrine half‐life fell from 11.8 to 8.7 hr, by phenobarbital, from 13.8 to 8.9 hr, by rifampicin (600 mg), from 11.7 to 7.1 hr, and by rifampicin (1,200 mg), from 11.7 to 5.6 hr; the antipyrine clearance was increased after antipyrine by 30%, after phenobarbital, by 56%, after rifampicin (600 mg), by 59%, and after rifampicin (1,200 mg), by 125%. D‐Glucaric acid excretion in urine showed a tendency to rise to the same extent in each group, while the γ‐glutamyl‐transpeptidase values were affected similarly after antipyrine and phenobarbital but remained unchanged after rifampicin. The 6‐β‐hydroxycortisol urinary excretion corrected by the 17‐hydroxycorticosteroids increased in all groups. There were no changes in plasma cholesterol, triglyceride, and other plasma lipids measured, and lipid electrophoresis was unchanged. Steady‐state plasma concentrations of cholesterol and plasma triglycerides were not elevated after induction of the microsomal enzyme system by the drugs used.