Perez G O, Oster J R, Sonneborn R E, Magrinat G, Vaamonde C A
J Pharmacol Exp Ther. 1977 May;201(2):456-62.
Renal acidification was studied in 12 lithium carbonate-treated psychiatric patients. The urinary Pco2 response to oral sodium bicarbonate loading, a qualitative index of distal hydrogen ion secretion, was evaluated in all patients and the results were compared with those obtained in 10 control subjects. The average maximal urine to arterial blood Pco2 difference (U-A Pco2) in the psychiatric patients [26 +/- 3 (S.E.) mm Hg] was significantly lower (P less than .001) than that of control subjects (51 +/- 3 mm Hg) and only three patients had values greater than 31 mm Hg (2 S.D. below the mean control value). Eight of these patients were also evaluated with NH4CL acid loading. Seven of eight patients had a minimal urine pH less than 5.30 after NH4CL administration; only one of the seven had a normal U-APco2 after bicarbonate loading. Three patients were evaluated prior to treatment and after 2 weeks of lithium administration. Pretreatment U-APco2 values were normal. After therapy the values were lower in all three patients becoming definitely abnormal in two. The present investigation, in concert with previous animal studies, demonstrates that chronic lithium carbonate therapy in man may result in decreased U-A Pco2.
对12例接受碳酸锂治疗的精神病患者的肾脏酸化功能进行了研究。评估了所有患者口服碳酸氢钠负荷后尿二氧化碳分压的反应，这是远端氢离子分泌的定性指标，并将结果与10名对照受试者的结果进行了比较。精神病患者的平均最大尿-动脉血二氧化碳分压差值（U-A Pco2）[26±3（标准误）mmHg]显著低于（P＜0.001）对照受试者（51±3 mmHg），只有3例患者的值大于31 mmHg（比对照均值低2个标准差）。其中8例患者还接受了氯化铵酸负荷试验。8例患者中有7例在给予氯化铵后最低尿pH值小于5.30；这7例患者中只有1例在碳酸氢盐负荷后U-APco2正常。对3例患者在治疗前和给予锂治疗2周后进行了评估。治疗前U-APco2值正常。治疗后，所有3例患者的值均降低，其中2例明显异常。本研究与先前的动物研究一致，表明人类长期接受碳酸锂治疗可能导致U-A Pco2降低。
