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PubMed1981

Digoxin in the elderly and in renal failure. Contribution of erythrocyte 86-rubidium uptake tests.

Na+,K+-ATPase activity was assessed indirectly in three groups of subjects of differing age, and in a group of patients with renal failure, by measuring the 86-rubidium uptake in the patients' own erythrocytes. The inhibiting action of digoxin on this activity was also measured in vitro. Erythrocyte 86Rb uptake was found to be lower in the elderly as was the calculated volume of distribution of digoxin. Sensitivity to the inhibiting action of digoxin increased with age. In the renal failure group 86Rb uptake was diminished and the sensitivity to digoxin was variable. This suggested that Na+,K+-ATPase activity could be one determinant of the volume of distribution of digoxin and that quantitative and qualitative changes of this enzyme could explain features of the pharmacokinetics of digoxin in renal failure and in old age.

Adult↗
PubMed1982

Modulation of murine in vitro erythroid and granulopoietic colony formation by ouabain, digoxin and theophylline.

Ouabain has been shown to increase the number of clonally derived erythroid stem cells, CFUE and BFUE, from normal murine bone marrow. We report here that digoxin and theophylline also enhance erythroid stem cell colony formation, in the presence of suboptimal concentrations of erythropoietin (Ep) (0.01 IU/ml) in methylcellulose culture. Both digoxin and theophylline increased CFUE colony formation optimally at 10(-8) M (29-81% respectively). The increase in BFUE colony formation occurred at 10(-10) M (35-76% respectively), suggesting that BFUE are more sensitive to the enhancing properties of these compounds. In addition, digoxin theophylline and ouabain were effective inhibitors of clonally derived granulocyte-macrophage progenitor cells, CFUC, from normal murine marrow plated in double layer agar in the presence of 10% L-cell conditioned medium (LCM). The degree of reduction in colony formation by CFUC ranged from 11% to 100%. Digoxin and theophylline were inhibitory for CFUC in the range of 10(-2) to 10(-12) M; however, ouabain was inhibitory over a broader concentration range of 10(-4) to 10(-18) M, suggesting that ouabain has a greater influence on committed hematopoietic progenitor cell colony formation. Both ouabain and digoxin have the property of binding to Na+/K+ATPase. This may mediate the alteration of hematopoietic differentiation. Theophylline, an adenyl cyclase inhibitor, may act through alterations in cyclic nucleotide levels. These studies further indicate that digoxin, theophylline and ouabain may serve as useful tools in elucidating the underlying mechanisms of how specific growth factors influence hematopoietic growth and differentiation.

Animals↗
PubMed1984

Pulmonary vascular response to digoxin in newborn lambs.

The effects of digoxin on pulmonary vascular resistance (PVR) were evaluated in normoxic (N) and hypoxic (H) newborn lambs with normal and elevated PVR, respectively. Lambs were anesthetized and instrumented to enable continuous measurement of mean pulmonary arterial pressure (PPA), mean left atrial pressure (PLA), mean pulmonary blood flow (Qp), and mean aortic pressure (PAO). Digoxin (10-20 micrograms/kg) was injected via central venous catheters in 11 N lambs and 4 H lambs. Under N conditions, baseline PVR was equal to 0.12 mm Hg/ml/min/kg, PPA was 33 mm Hg, PLA was 6 mm Hg, Qp was 235 ml/min/kg, and PAO was 69 mm Hg. Following digoxin, mean PVR increased by 24% (P less than 0.001) and PPA increased by 23% (P less than 0.001) for an average duration of 199 sec while QP increased by 5% (P less than 0.02) and PLA was constant suggesting a direct vasoconstrictive effect. Under H conditions, baseline PVR was equal to 0.26 mm Hg/ml/min/kg, PPA was 58 mm Hg, PLA was 4 mm Hg, Qp was 208 ml/min/kg, and PAo was 65 mm Hg. Following digoxin, mean PVR, Qp, PLA, and PAo did not change appreciably although PPA had a uniform increase of 5% (P less than 0.001). The blunted response may suggest that either the pulmonary vascular bed was maximally constricted or that digoxin and hypoxia share a common mechanism. In conclusion, digoxin has a direct pulmonary vasoconstrictor action in newborn lambs. Because of its short duration, this action probably should not alter the clinical use of this drug in newborn humans.

Animals↗
PubMed1978

Influence of soft gelatin on digoxin absorption.

1 The influence of encapsulation in soft gelatin on the absorption of digoxin from a solvent mixture of polyethylene glycol 400 90% W/W, ethanol 6% W/W, propylene glycol 3% W/W and water 1% W/W was studied in eight healthy volunteers. 2 Each volunteer received 0.6 mg digoxin as solution alone, as three intact capsules containing digoxin solution, as three capsules containing digoxin solution sectioned in half and as three capsules containing digoxin solution dissolved in water prior to administration. 3 There was no significant difference between the four treatments in terms of area under the plasma concentration--time curves for 7 h, peak plasma concentrations, time to peak or in the cumulative urinary excretion for 6 days. 4 It is suggested that a constituent of the solvent rather than the presence of or encapsulation within soft gelatin may be the determining factor in enhanced absorption of digoxin from soft gelatin capsules as compared to aqueous solution or tablets of rapid dissolution rate.

Adult↗
PubMed1984

Digoxin in dogs: once a day or twice a day?

Healthy mature dogs were given digoxin orally at the same dose once a day (SID) or divided (BID) at 12-hour intervals. Blood concentrations of digoxin were determined by radioimmunoassay. When the drug was given SID, peak blood concentrations were higher than, but lowest blood concentrations were not different than, those obtained when the drug was given BID. Thus, average blood concentration throughout 24 hours was significantly (P less than 0.05) greater when digoxin was given SID than when given BID. This suggested a reduced rate of clearance and an increased risk for toxicosis for digoxin when given SID versus BID. Peaks of digoxin blood concentrations were lower when the drug was given BID rather than SID; however, we do not know whether the smaller fluctuations can be translated into greater efficacy and/or less toxicity. Unless those questions are answered, we recommend that digoxin be administered BID to mature dogs.

Animals↗
PubMed1978

Interaction between quinidine and digoxin.

The serum digoxin concentration increased in 25 of 27 study patients (93%), and the mean serum digoxin concentration rose from 1.4 ng/ml to 3.2 ng/ml during quinidine therapy. Anorexia, nausea, or vomiting developed in 16 patients (59%) but disappeared in all ten patients for whom the digoxin dose alone was reduced, suggesting that digoxin excess caused these symptoms. Ventricular premature depolarizations developed in three patients after starting quinidine therapy; ventricular tachycardia developed in one patient, and another died suddenly. When starting quinidine therapy in patients who are taking digoxin, the clinical course, ECG, and serum digoxin level should be followed closely.

Aged↗
PubMed1978

Multidisciplinary audit of digoxin.

Use review of digoxin as part of a medical care evaluation study in a hospital is described. This drug audit within the hospital's quality assurance program used a multidisciplinary approach. The study was designed to measure the incidence of digoxin toxicity, evaluate monitoring practices for digoxin use and evaluate the adequacy of digoxin dosing patterns. Forty-eight patients were involved. Results indicated that some patients were not adequately assessed in regard to renal function and digoxin serum level. Further, there was a 17% incidence of digoxin toxicity. Studies such as this give pharmacists an opportunity to use their knowledge of proper drug use through a structured hospital program.

Adult↗
PubMed1978

Estimation of serum digoxin levels in geriatric patients.

The correlation in geriatric patients between estimated serum digoxin levels based on pharmacokinetic calculations and serum digoxin levels measured by radioimmunoassay was studied. Serum digoxin levels were estimated for 17 geriatric patients recieving digoxin using the "total body stores" concept. A statistically significant correlation between calculated and measured digoxin levels was shown (p less than 0.05, r = 0.51); however, 95% confidence limits were so large (+/- 1.75 ng/ml) that the results were clinically unacceptable. Until data describing specific causes of variance are available and calculations modified to account for specific variations, pharmacokinetic models should not be relied upon for accurate estimates of digoxin levels in geriatric patients.

Aged↗
PubMed1977

Development and evaluation of an individualized patient education program about digoxin.

A study was undertaken to (1) develop an individualized audiovisual patient education program about digoxin and congestive heart failure, and (2) ascertain whether a patient who received the education program from a pharmacist would demonstrate a significantly greater gain in knowledge about digoxin and congestive heart failure than a traditionally-educated patient. The education program consisted of a slide/tape audiovisual presentation which was reinforced by the pharmacist presenting the program at the patient's bedside. Each patient was randomly assigned to either the study group or control group of patients. A 27-question pretest was given to both the control and study groups of patients to determine their baseline knowledge of congestive heart failure and digoxin therapy. Only the study group of patients received the individualized education program. All patients were then given a posttest to determine the degree of learning that took place during their hospital stay. The patients who received the individualized digoxin education program from a pharmacist demonstrated a significantly greater gain in knowledge about digoxin and congestive heart failure than traditionally-educated patients. It is suggested that hospital pharmacists should deliver an individualized education program to patients taking digoxin during their hospital stay.

Audiovisual Aids↗
PubMed1978

Age dependant factors influencing digoxin pharmacokinetics in the postnatal puppy.

H3-digoxin pharmacokinetics following intravenous pulse injections was studied in dogs ranging in age from 0.5--2 days (n=2), 3--10 days (n=6), 11--30 days (n=5), 31--90 days (n=3) and adult dogs (n=5). All animals in each age group exhibited a biexponential elimination of H3-digoxin from the vascular compartment and data are analyzed by use of a two compartment pharmacokinetic model. Pharmacokinetic parameters showed significant age related differences. The mean T1/2(alpha) was greater in puppies aged 0.5--2 (8.92 +/- 2.61 min), 3--10 (11.8 +/- 1.99 min) and 11--30 days (10.32 +/- 1.89 min) when compared to adult dogs (5.36 +/- 0.91 min). The mean T1/2(beta) was four times longer in 3--10 day old dogs (1342.05 min) than in adult dogs (327.0 min) and decreased with increasing age of the puppies. The beta-phase rate constants were statistically different (p less than 0.05) between 3--10 day old and adult dogs. Elimination of H3-digoxin was slower in puppies than adult dogs (Kel in 3--10 day old puppies = 0.0046 min(-1); adult dogs = 0.0197 min(-1)) and was accompanied by a lower clearance of H3-digoxin in 3--10 day old puppies (2.05 ml/min/kg) than in adult dogs (7.41 ml/min/kg) [p less than 0.0001]. Functional immaturity of the canine kidney during early development probably constitutes the physiologic basis for the differences noted in H3-digoxin kinetics. While these distinctions in elimination kinetics are age related they do not clarify why younger organisms tolerate higher digoxin levels than adults with less apparent toxicity.

Age Factors↗
PubMed1983

Modification of digoxin induced arrhythmogenicity in adult rats following atropine administration.

Atropine alone in the two lower doses (20mg/kg and 40mg/kg) did not produce any arrhythmias while 80mg/kg of atropine produced arrhythmias in 33% of animals after 31.0 +/- 7.5 min. Only 11% of these rats developed paroxysmal atrial tachycardia. Atropine in lower doses (20,40mg/kg) with digoxin (40mg/kg) decreased the total percent of digoxin induced arrhythmias, delayed their onset, and changed the type of arrhythmias as compared with the digoxin group alone. Atropine given in higher dosage (80mg/kg) with digoxin (40mg/kg) produced arrhythmias in 100% of rats as did digoxin alone, but significantly shortened their onset and modified the types of arrhythmias seen. In conclusion, atropine in varying doses significantly modified digoxin toxicity.

Animals↗
PubMed1980

Digoxin without effect on renin release in healthy subjects.

In the clinical evaluation of renin status, the effect of chronic digitalization is unknown. A 50 per cent decrease in PRA is presented after intravenous digoxin injection. In this study the acute intake of 0.75 mg digoxin decreased PRA slightly (p less than 0,05), but no difference could be found in ten healthy volunteers in regard to PRA after placebo, randomly examined twice after digoxin and once after placebo tablets. Eight healthy volunteers were digitalized with 2.5 mg digoxin in total during four days. Renin release was stimulated by ergometric exercise (900 kpm for 10 min) before and after digitalization, when the mean serum digoxin concentration was 2.0 +/- 0.2 ng/ml (SEM). No difference in basal or exercise-stimulated PRA could be found after digoxin. We conclude that the steady state digitalis therapy does not interfere with renin release. The peripheral vasoconstriction accompanied with the acute intravenous digitalis administration can lead to a transient decrease of PRA.

Adult↗
PubMed1980

[Comparative evaluation of different kits for serum digoxin determination (author's transl)].

In the last years the determination of serum digoxin levels has become absolutely necessary not only in specialized centers but also in all medical departments for its pharmacological and clinical implications. In order to verify the reproducibility, accurateness and sensibility of the techniques currently employed we performed a comparative analysis of the serum digoxin levels obtained by using one immuno-enzymatic and four different radio-immuno-assay kits. The first in vitro trial was performed by evaluating serum digitalis on blood specimens from eight healthy human donors to which known doses of digoxin and beta-methyl-digoxin had been added. The second in vivo trial was performed by giving for three days to sixteen cardiac patients, previously off any digitalis treatment, only one oral morning dose of 0.125 mg of digoxin (8 patients), and 0.135 mg of beta-methyl-digoxin (8 patients). A monoexponential decay constant was calculated on the curves of serum digitalis levels, measured in the third day of treatment by means of the five different techniques. The statistical analysis, performed on the results we obtained, demonstrates a satisfying degree of reproducibility and accurateness only for some of the kits used. This is due to a poor sensibility of some kits in the presence of low digitalis levels, which can produce significantly different value for the decay constant (p < 0.02). Such a behaviour possibly due to different manufacturing processes of the kits raises some questions on the validity in comparing results from various laboratories when different testing procedures are employed.

Digoxin↗
PubMed1981

[Radioimmunoassay of serum digoxin levels. Technical aspects (author's transl)].

This work analyses, in a first part, radioimmunoassay of serum digoxin levels in more than 4 500 patients during a period of 4 years using the same kit. A preliminary step of this work was to test the kits available 4 years ago i.e a kit using (3H) digoxin and 3 kits using (125I) digoxin. Results about this choice are summarized. The (3H) kit was finally chosen. It was used with slight modifications of the original protocol. This kit was as sensitive as 0.25 ng/ml and was specific for digoxin and its related derivatives. The reproducibility agrees with results in literature. Serum digoxin levels were assayed in the same samples, both with the (3H) kit and (125I) kits. Under these conditions, a lower average value was found with the former system. This result points out that the labelling protocol of the digoxin can modify the apparent normal therapeutic value observed when radioimmunoassay is done with different kits.

Animals↗
PubMed1982

The development and application of a radioimmunoassay for dihydrodigoxin, a digoxin metabolite.

The cardioinactive digoxin metabolite, dihydrodigoxin, has been conjugated to bovine serum albumin and to bovine pancreatic ribonuclease by the periodate oxidation method. Rabbits immunized with the dihydrodigoxin-bovine serum albumin conjugate formed antibodies which bound a radioiodinated dihydrodigoxin-ribonuclease conjugate. This binding was inhibited by dihydrodigoxin. After affinity chromatography on a digoxin-ribonuclease-Sephacryl immunoadsorbent to remove antibodies which cross-reacted with digoxin, dihydrodigoxin was 300 times more effective than digoxin in inhibiting the binding of tracer by antibody. Digoxin-absorbed antidihydrodigoxin antibodies were coupled to Sephacryl and were used to develop a solid-phase radioimmunoassay capable of detecting 250 to 500 pg of dihydrodigoxin in 1 ml of human serum or urine. This radioimmunoassay has been used to define the pharmacokinetics of the metabolite in four normal human volunteers who ingested 125 to 500 micrograms of dihydrodigoxin by mouth. Dihydrodigoxin was quickly absorbed, with maximal serum concentrations achieved within 45 to 105 min, followed by a rapid fall in serum immunoreactivity over 2 to 4 hr and then by a slower, more gradual decline. The terminal half-life (beta) in serum varied from 4.24 to 11.9 hr (mean +/- S.E. = 8.1 +/- 1.3 hr). Most of the administered dose was excreted in the urine, with cumulative urinary recovery varying inversely with the dose. Urinary half-lives averaged 13.8 +/- 2.1 hr, and renal clearance rates were similar to those of creatinine. Dihydrodigoxin is rapidly absorbed and excreted in man and appears to be eliminated from the body at a faster rate than digoxin.

Adult↗
PubMed1982

Complications associated with digoxin therapy in low-birth weight infants.

Eighteen infants, each weighing less than 1,500 gm, were treated with low dose digoxin therapy for patent ductus arteriosus and signs of circulatory congestion. Nine of the 18 developed one or more signs of clinical deterioration felt to be related to digoxin therapy: eight infants experienced frequent episodes of bradycardia, six had cardiac arrhythmias, and six experienced feeding difficulties. All signs disappeared when digoxin therapy was discontinued. Digoxin, even in relatively low dosages, can have deleterious complications in seriously ill low-birth-weight infants. Alternatives to digoxin in this patient population should be considered before institution of digoxin therapy.

Arrhythmias, Cardiac↗
PubMed1982

Pharmacokinetics of digoxin in low-birth-weight infants.

Digoxin pharmacokinetics were studied in 13 low-birth-weight infants requiring digoxin therapy. Their weights ranged from 820 to 2,710 g (mean = 1,440 g) and gestational ages ranged from 26 to 38 weeks (mean = 30.9 weeks). The distribution and elimination of digoxin can be described by an open two-compartment model. Poor correlation between volume of distribution Vd beta 95.7 +/- 1.0 liters/kg) and gestational age (GA) or weight (Wt) was observed. Digoxin half-life (47 +/- 21 h) was inversely related to GA and Wt (r = 0.69 and 0.66, respectively), but total body digoxin clearance (29.8 +/- 14.7 ml/min/1.73 m2) was found to be highly dependent on these two variables (r = 0.87 and 0.88, respectively). According to the results of this study and our previous investigation, digitalizing and maintenance dosages of digoxin were recommended.

Digoxin↗
PubMed1980

A two-compartment model for digoxin disposition in dogs.

The disappearance of digoxin from heart and skeletal muscle was studied in dogs using a sequential biopsy technique. The animals were injected with digoxin for five days and subsequently with 3H-digoxin for an additional three days. 12, 24, and 48 h after discontinuation of digoxin, tissue samples of left ventricle, left atrial appendage, and skeletal muscle were taken. In addition, digoxin serum levels were measured. With the help of a computer program, a mathematical model was developed for the description of the disposition and elimination of digoxin from tissue. Disappearance from plasma and tissue was consistent with a two-compartment open model.

Animals↗