Basseches P J, DiGregorio G J
Arch Int Pharmacodyn Ther. 1982 Jun;257(2):180-7.
The excretion of the widely used antiarrhythmic agent procainamide into the bile and saliva of rats with chronic renal failure (CRF) induced by a two stage-total nephrectomy was studied. Chronic renal failure significantly elevates plasma, salivary, and biliary procainamide levels compared to normal and sham operated rats at all time periods studied. However, while the increase in salivary excretion parallels that of plasma, biliary excretion does not. Results indicate that there is probably saturation of an active transport mechanism for procainamide into bile and that bile cannot compensate for increased drug levels which accumulate during CRF. Salivary excretion, though increased during CRF, also cannot compensate for elevated procainamide levels. Moreover, CRF does not appear to impair non-microsomal acetylation of procainamide, the major biotransformation reaction in the metabolism of this drug.
研究了通过两阶段全肾切除术诱导慢性肾衰竭（CRF）大鼠对广泛使用的抗心律失常药物普鲁卡因胺的胆汁和唾液排泄情况。与正常大鼠和假手术大鼠相比，在所有研究时间段内，慢性肾衰竭均显著提高了血浆、唾液和胆汁中普鲁卡因胺的水平。然而，虽然唾液排泄的增加与血浆平行，但胆汁排泄并非如此。结果表明，普鲁卡因胺进入胆汁的主动转运机制可能存在饱和，并且胆汁无法补偿慢性肾衰竭期间积累的药物水平升高。唾液排泄虽然在慢性肾衰竭期间增加，但也无法补偿普鲁卡因胺水平的升高。此外，慢性肾衰竭似乎并未损害普鲁卡因胺的非微粒体乙酰化，这是该药物代谢中的主要生物转化反应。
