Williamson P J, Ene M D, Roberts C J
Br J Clin Pharmacol. 1984 Oct;18(4):619-23. doi: 10.1111/j.1365-2125.1984.tb02515.x.
Ten healthy individuals received frusemide 40 mg orally for 7 days. Following a drug free period of 7 days they received azapropazone 600 mg twice daily for 7 days and then both treatments for a further 7 days. Sodium excretion fell from 141 +/- 16.8 mmol/day to 84.3 +/- 6.8 mmol/day (P less than 0.01) on initiation of azapropazone treatment. The natriuretic response to frusemide was unchanged by premedication with azapropazone. Urate excretion rose from 3.35 +/- 0.249 mmol/day to 4.98 +/- 0.365 mmol/day on initiation of azapropazone therapy but subsequently returned to baseline values. Plasma uric acid fell from 0.289 +/- 0.024 mmol/l to 0.167 +/- 0.0125 mmol/l (P less than 0.001) on azapropazone but rose to 0.186 +/- 0.0116 mmol/l (P less than 0.001) with the addition of frusemide. Azapropazone may cause sodium retention but after repeated administration frusemide still has a marked diuretic action. The hypouricaemic effect of azapropazone is only slightly antagonised by frusemide at the doses studied.
10名健康个体口服40毫克速尿,持续7天。在7天的停药期后,他们每天两次服用600毫克阿扎丙宗,持续7天,然后两种治疗再持续7天。开始阿扎丙宗治疗时,钠排泄量从141±16.8毫摩尔/天降至84.3±6.8毫摩尔/天(P<0.01)。阿扎丙宗预处理对速尿的利钠反应没有影响。开始阿扎丙宗治疗时,尿酸排泄量从3.35±0.249毫摩尔/天升至4.98±0.365毫摩尔/天,但随后恢复到基线值。服用阿扎丙宗时,血浆尿酸从0.289±0.024毫摩尔/升降至0.167±0.0125毫摩尔/升(P<0.001),但加用速尿后升至0.186±0.0116毫摩尔/升(P<0.001)。阿扎丙宗可能会导致钠潴留,但重复给药后速尿仍有明显的利尿作用。在所研究的剂量下,速尿对阿扎丙宗的降尿酸作用仅有轻微拮抗。