Influence of Potassium Depletion on Myocardial Concentration of Tritiated Digoxin

• Published in: Circulation research 1967-05, Vol.20 (5), p.473-476
• Main Authors: Cohn, Keith E, Kleiger, Robert E, Harrison, Donald C
• Format: Article
• Language: English
• Subjects: Acute Kidney Injury - metabolism; Animals; Digitalis - metabolism; Digoxin - metabolism; Hypokalemia - metabolism; Membrane Potentials; Mice; Myocardium - metabolism; Plants, Medicinal; Plants, Toxic; Potassium Deficiency - metabolism; Tritium
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.RES.20.5.473

The influence of potassium deficiency on myocardial H-digoxin concentration in the mouse was studied. Tritiated digoxin, 400 μg/kg, was injected intraperitoneally into mice, which were killed at varying time intervals, and the H-digoxin was extracted. One-half of the mice were made potassium deficient by a diet free of potassium.In control animals, myocardial H-digoxin was maximal by 30 min and declined through 24 hours. There was no significant difference between the myocardial H-digoxin of the control and potassium-depleted groups at ½ 1, 2, 6, or 16 hours, but at 24 hours a significantly higher concentration of digoxin was present in the potassium-deficient mouse hearts (23.6 ± 5.2 mμg/g) than in the control group (3.1 ± 1.5 mμg/g). Potassium-depleted mice with total renal failure, produced by bilateral ligation of the renal pedicle, showed increased myocardial H-digoxin levels at 20 hours as compared with mice with renal failure but without potassium deficiency.It is concluded that potassium deficiency may lead to increased concentrations of cardiac digoxin. The findings in the anuric animals suggest that diminished renal function produced by potassium depletion is not the sole mechanism of this retention of cardiac H-digoxin.