Beeinflussung der Erythrocyten-Elektrolyte durch ?-Methyl-Digoxin bei Gesunden

Abstract

6 healthy controls received daily doses of 0.6 mg beta-methyl-digoxin for 3 days and further 0.3 mg for the following 5 days each. After the first 3 days sodium content in the red cells increased from 4.8 to 6.6 meg/kg significantly in parallel to the glycoside level of 1.5 ng/ml (1.2 times 10-9 M). At the same time magnesium in the cells fell significantly from 4.1 to 3.7 meg/kg. There was no change in the concentration of potassium, calcium or chloride at this time. While the glycoside level dropped during the following 5 days under 0.3 mg of methyl-digoxin to 1.2 ng/ml (1 times 10-9 M), sodium content in the cells increased further up to 8.3 meq/kg and was paralleled by a decrease in potassium content from 84.6 to 82.0 meq/kg. There were no changes in plasma electrolyte concentrations during the experiments. Our results confirm the concept of Hoffman that there are two transport pathways in human red cells which differ basically in their dependencies of the sodium and potassium composition of the external medium and the concentration of glycoside needed to inhibit the transport. Our data evidence that red cell electrolyte contents reflect levels of digoxin. They might be useful to follow up the therapeutical effect of cardiac glycosides.

Influence of digitalis and diuretics on ouabain binding sites on human erythrocytes

“…Thus, the inhibition of this system will cause an altered transport rate across the cell membrane for Na + and K +. In fact, an inhibition of active cation transport rate and, as a consequence, increased intra-erythrocytic Na+-concentrations and decreased K +-concentrations have been measured in patients on cardiac glycoside treatment [2,8,25]. If chronic hypokalemia results in an increased number of (Na + + K +)-ATPase molecules (and ouabain binding sites), there should be an increased transport capacity of the cell membrane for Na + and K +.…”