Brater D C
Clin Pharmacol Ther. 1979 Mar;25(3):322-30. doi: 10.1002/cpt1979253322.
The effects of indomethacin-induced prostaglandin inhibition on sodium and chloride homeostasis in normal man were assessed. Seven normal subjects were on a 150-mEq sodium diet for 3 days prior to receiving indomethacin or no drug. Indomethacin decreased fractional excretions of sodium and chloride without affecting fractional excretion of potassium, creatinine clearance, or percent fractional reabsorption of free water. Cumulative sodium excretion at 8 hr fell from 49.8 +/- 7.2 to 16.1 +/- 4.8 mEq (p less than 0.005) after indomethacin. Chloride fell at 8 hr from 49.7 +/- 6.4 to 21.3 +/- 5.1 mEq (p less than 0.005). Urinary volume and osmolal clearance decreased in similar magnitudes such that free water reabsorption was not changed by indomethacin. This study showed that indomethacin decreased renal sodium and chloride excretion, implying that endogenous prostaglandins may be modulators of renal sodium excretion.
评估了消炎痛诱导的前列腺素抑制对正常人体内钠和氯稳态的影响。七名正常受试者在接受消炎痛或无药物治疗前,先进行了3天的150毫当量钠饮食。消炎痛降低了钠和氯的分数排泄,而不影响钾的分数排泄、肌酐清除率或自由水的分数重吸收百分比。消炎痛给药后8小时的累积钠排泄量从49.8±7.2毫当量降至16.1±4.8毫当量(p<0.005)。8小时时氯从49.7±6.4毫当量降至21.3±5.1毫当量(p<0.005)。尿量和渗透清除率下降幅度相似,因此消炎痛并未改变自由水重吸收。这项研究表明,消炎痛降低了肾脏钠和氯的排泄,这意味着内源性前列腺素可能是肾脏钠排泄的调节剂。