Abe Y, Sekiguchi H, Tsuru K, Irikura T
Nihon Yakurigaku Zasshi. 1984 Apr;83(4):317-24.
Effects of 3,4,5-trimethoxy-N-(3-piperidyl) benzamide (KU-54), an antiulcer drug, on the tissue respiration of the gastric mucosa and the liver were studied in rats. Oral KU-54 at 100 mg/kg twice daily for 5 days (though it was given only once on the 5th day) caused an increase in oxygen consumption of the gastric mucosa in rats, but did not affect that of the liver. Thus the principal active site of KU-54 on tissue respiration was found to be the gastric mucosa. Oral KU-54 at 100 mg/kg once daily for 11 days significantly accelerated the oxygen consumption of marginal gastric mucosa of acetic acid ulcer in rats. The effect of oral gefarnate at 200 mg/kg was about half that of KU-54 at 100 mg/kg, but it was not significant. In addition, oral KU-54 at 100 mg/kg twice daily for 5 days (though it was given only once on the 5th day) significantly inhibited the decrease of oxygen consumption of the gastric mucosa in hemorrhagic shocked rats. The effect of oral gefarnate at 100 mg/kg was not like that at KU-54 at 100 mg/kg in conscious rats. When KU-54 was added in the incubation medium with small gastric mucosal fragments of rats, the increase of oxygen consumption of the gastric mucosa did not occur. Oral KU-54 at 100 mg/kg significantly accelerated a glycogen consumptive stimulation of the gastric mucosa of the corpus in ischemic rats, but the respiration of the antral mucosa was not accelerated under anaerobic incubating conditions. Oral gefarnate at 200 mg/kg accelerated an anaerobic glycolysis of the gastric antral mucosa in rats.
研究了抗溃疡药物3,4,5-三甲氧基-N-(3-哌啶基)苯甲酰胺（KU-54）对大鼠胃黏膜和肝脏组织呼吸的影响。大鼠每日两次口服100mg/kg KU-54，共5天（尽管第5天仅给药一次），可使大鼠胃黏膜耗氧量增加，但对肝脏耗氧量无影响。因此，发现KU-54对组织呼吸的主要作用部位是胃黏膜。大鼠每日一次口服100mg/kg KU-54，共11天，可显著加速乙酸溃疡大鼠胃边缘黏膜的耗氧量。口服200mg/kg吉法酯的效果约为100mg/kg KU-54的一半，但不显著。此外，大鼠每日两次口服100mg/kg KU-54，共5天（尽管第5天仅给药一次），可显著抑制失血性休克大鼠胃黏膜耗氧量的降低。在清醒大鼠中，口服100mg/kg吉法酯的效果与100mg/kg KU-54的效果不同。当在含有大鼠小胃黏膜碎片的孵育培养基中加入KU-54时，胃黏膜耗氧量未增加。大鼠每日一次口服100mg/kg KU-54，可显著加速缺血大鼠胃体黏膜的糖原消耗刺激，但在厌氧孵育条件下，胃窦黏膜的呼吸未加速。口服200mg/kg吉法酯可加速大鼠胃窦黏膜的无氧糖酵解。
