Why the study?
Does short-term digoxin treatment alter erythrocyte glycoside receptor sites, rubidium uptake, and sodium concentrations in patients with heart failure or atrial fibrillation?
Does short-term digoxin treatment alter erythrocyte glycoside receptor sites, rubidium uptake, and sodium concentrations in patients with heart failure or atrial fibrillation?
Erythrocyte digoxin binding and rubidium uptake correlate with cardiac response to digoxin better than plasma digoxin concentrations.
Answers are grounded in this paper and cite their sources.
Erythrocyte digoxin binding and sodium changes associate with early cardiac response where plasma levels do not; leaves open their utility for monitoring in HF or AF.
1 Measurements of the binding of 12-alpha-[3H]-digoxin to the membranes of intact erythrocytes, erythrocytic 86rubidium uptake and intraerythrocytic sodium concentrations have been made in the red cells of patients receiving digoxin in the short-term for atrial fibrillation or cardiac failure in regular rhythm. 2 During the first few days of treatment [3H]-digoxin binding and 86rubidium uptake fall and intraerythrocytic sodium concentrations rise. 3 Subsequently parallel fluctuations occur in [3H]-digoxin binding and 86rubidium uptake but not in intraerythrocytic sodium concentrations and the significance of the fluctuations is discussed. 4 The values of all three measurements correlate significantly with the response of the heart in sinus rhythm as measured by QS2I. 5 Plasma digoxin concentrations do not correlate with QS2I.
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Ford et al. (1979) studied this question.
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