Pentiuk A A, Bogdanov N G, Lutsiuk N B
Vopr Pitan. 1987 Mar-Apr(2):50-3.
Group I rats were given orally syncumar (1.5 mg/kg/day) during 5 days to induce K-avitaminosis. Group II and III animals received vikasol, a synthetic analogue of vitamin K (3 and 30 mg/kg/day, respectively), during 6 days. Delayed biotransformation of amidopyrine was recorded in the animals with vitamin K deficiency. The total 4-aminoantipyrine excretion was reduced due to a steady decrease in the excretion of both free form of this substance and its acetylated metabolite. Delayed conversion of benzoic acid into hippuric acid and benzoyl glucuronides was noted in rats with K-avitaminosis. Vikasol administration stimulated biotransformation of amidopyrine and benzoic acid, the low doses of vikasol (3 mg/kg) being more effective as compared to the high doses (30 mg/kg).
第一组大鼠在5天内口服新抗凝（1.5毫克/千克/天）以诱导维生素K缺乏症。第二组和第三组动物在6天内分别接受维生素K的合成类似物维生素K3（3毫克/千克/天和30毫克/千克/天）。在维生素K缺乏的动物中记录到氨基比林的生物转化延迟。由于该物质游离形式及其乙酰化代谢物的排泄稳定减少，4-氨基安替比林的总排泄量降低。在维生素K缺乏症大鼠中，观察到苯甲酸向马尿酸和苯甲酰葡糖醛酸的转化延迟。给予维生素K3刺激了氨基比林和苯甲酸的生物转化，低剂量的维生素K3（3毫克/千克）比高剂量（30毫克/千克）更有效。
