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Biomedical subjects

J K Aronson

Publications and source records attributed to J K Aronson.

136 records · Page 8Linked to original sources
PubMed1979

The acute changes seen in cardiac glycoside receptor sites, 86rubidium uptake and intracellular sodium concentrations in the erythrocytes of patients during the early phases of digoxin therapy are not found during chronic therapy: pharmacological and therapeutic implications for chronic digoxin therapy.

1 Measurements of the binding of 12-alpha-[3H]-digoxin to the membranes of intact erythrocytes, erythrocyte 86rubidium uptake and intraerythrocytic sodium concentrations have been made in the red cells of various groups of patients--those who have not received digoxin, those during the early phases of treatment, those during chronic (greater than 2 months) treatment, and those toxic. 2 The values of those measurements in the patients in the early phases of therapy and in the toxic patients differed significantly from those of the untreated patients. 3 However, the values in the chronically treated patients were not different from those of the untreated patients. 4 The results suggest that the biochemical pharmacological effects of digoxin which occur during the early phases of therapy do not persist in the long-term. 5 The possible clinical significance of these observations is discussed.

Aged↗
PubMed1978

Monitoring digoxin therapy: III. How useful are the nomograms?

1. A previously described set of guidelines for digoxin therapy has been evaluated in twenty-four patients. 2. Six different published methods (nomograms and equations) for predicting digoxin requirements have been studied to determine their clinical usefulness in the context of the twenty-four patients. 3. The limitations of the nomograms and equations are discussed.

Adult↗
PubMed1978

Monitoring digoxin therapy. The use of plasma digoxin concentration measurements in the diagnosis of digoxin toxicity.

The usefulness of measuring plasma digoxin concentrations in the diagnosis of digoxin toxicity has been assessed in 83 in-patients. The mean plasma digoxin concentration in clinically toxic patients was significantly higher than the mean concentration in non-toxic patients. The overlap between the groups, however, was extensive and could partly be accounted for by hypokalaemia in those toxic patients whose plasma digoxin concentration was less than 3 ng/ml. There was, in addition, a higher incidence of hyperkalaemia, without obvious cause, in toxic patients than in non-toxic patients. Consideration of the incidence of various non-cardiac factors, specifically plasma potassium concentration greater than 5.0 mmol/l, plasma creatinine concentration greater than 150 mumol/l, daily maintenance dose greater than 6 microgram/kg, and age greater than 60 years, led to the development of guidelines to aid in the diagnosis of digoxin toxicity. Patients with plasma digoxin concentration greater than 3 ng/ml or with hypokalaemia should be considered probably toxic and those with plasma digoxin concentration greater than or equal to 3 ng/ml in the absence of hypokalaemia should only be considered toxic if they have at least two of the non-cardiac factors outlined above. Plasma digoxin concentrations could not be predicted with more than 31 per cent certainty by considering the magnitude of those non-cardiac factors.

Aged↗
PubMed1977

Monitoring digoxin therapy: I. Plasma concentrations and an in vitro assay of tissue response.

1 An in vitro technique is described for measuring the uptake of 86Rb by human erythrocytes. 2 Fifteen patients were treated with digoxin for atrial fibrillation and other fast arrhythmias. 3 86Rb uptake by the patients' own red cells fell from pre-treatment values during digitalization. 4 The therapeutic response of patients with atrial fibrillation correlated better with the changes in 86Rb uptake than with plasma digoxin concentrations.

Adult↗
PubMed1977

Monitoring digoxin therapy: II. Determinants of the apparent volume of distribution.

1 In eighteen subjects receiving digoxin therapy the apparent volume of distribution (Vd) of the drug has been calculated. 2 For each subject the sensitivity of the 86Rb transport mechanism of his pre-treatment erythrocytes to in vitro inhibition by digoxin has been measured (IC50). 3 The Vd of digoxin correlates both with the age of the patients and with the IC50 of their pre-treatment erythrocytes. 4 The implications of these findings are discussed in terms of the possible determinants of the Vd of digoxin. 5 Digoxin requirements may be predictable before therapy commences if IC50 measurements are performed.

Adult↗