Garty M, Sood P, Rollins D E
Ann Intern Med. 1981 Jan;94(1):35-7. doi: 10.7326/0003-4819-94-1-35.
Elevated serum digoxin concentrations and clinical toxicity have been reported in patients receiving quinidine. The present study was undertaken to ascertain whether a similar interaction occurs between quinidine and another cardiac glycoside, digitoxin, and if so to evaluate the pharmacokinetic basis in five healthy volunteers. In the presence of quinidine the serum digitoxin concentration was elevated, the mean digitoxin elimination half-life was increased from 87.8 +/- 11.6 to 218.3 +/- 20.6 h (mean +/- SEM) (p < 0.01), and mean total body clearance was reduced from 5.01 +/- 1.18 to 1.87 +/- 0.20 mL/h x kg (p < 0.052). No change was observed in the apparent volume of distribution or in the volume of the central compartment for digitoxin. The data suggest that the mechanism for this interaction is a reduction in elimination and not displacement of digitoxin from tissue binding sites.
据报道,接受奎尼丁治疗的患者血清地高辛浓度升高且出现临床毒性。本研究旨在确定奎尼丁与另一种强心苷洋地黄毒苷之间是否会发生类似的相互作用,若存在相互作用,则评估其在5名健康志愿者体内的药代动力学基础。在使用奎尼丁的情况下,血清洋地黄毒苷浓度升高,洋地黄毒苷的平均消除半衰期从87.8±11.6小时增加至218.3±20.6小时(平均值±标准误)(p<0.01),平均全身清除率从5.01±1.18毫升/小时·千克降至1.87±0.20毫升/小时·千克(p<0.052)。洋地黄毒苷的表观分布容积或中央室容积未观察到变化。数据表明,这种相互作用的机制是消除减少,而非洋地黄毒苷从组织结合位点被置换。