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PubMedDate not supplied

The effects of exercise training on the pharmacokinetics of digoxin.

BACKGROUND: Studies have shown that digoxin binds to the working muscles during an acute bout of exercise, with a concomitant decrease in serum digoxin concentration. This study investigated the effects of 16 weeks of endurance exercise training on the pharmacokinetics of digoxin in old and young adults. METHODS: Twelve subjects, aged 68.5 +/- 4.5 years, and six subjects, aged 30.3 +/- 3.8 years, completed the study. All subjects were healthy, sedentary, and taking no cardiovascular medications. After initial testing and maximum oxygen consumption (VO2max) measurements, subjects were hospitalized for 28 hours for renal function testing and digoxin clearance studies and then randomly assigned to an exercise (EG) or control (CG) group. The EG completed 16 weeks (three 1-hour bouts/week) of aerobic training at 75% to 85% of maximum capacity. The CG did not exercise. All tests were repeated at the end of the 16-week study period. RESULTS: In the older EG subjects, VO2max increased by 3.4 ml/kg/min, or approximately 16% (P = 0.0002). VO2max increased in the younger EG subjects by 1.1 ml/kg/min, but the increase was not significant (P > 0.05). There were no significant changes in body composition, renal function, or time of onset, peak concentration, or elimination phase half-life of digoxin in either the old or young exercise or control groups (P > 0.05 for all variables). CONCLUSION: Although 16 weeks of endurance exercise training improves cardiorespiratory fitness, the pharmacokinetics of digoxin are neither improved nor adversely affected in healthy old and young adults.

Adult↗
PubMed1981

Is maintenance digoxin necessary in geriatric patients?

Digoxin therapy was withdrawn over a four-year period in the geriatric wards of Skellefteå Hospital, if the indications for it were not clear, the medication was of doubtful value and there were no contraindications to withdrawal. Contraindications comprised symptoms of cardiac failure at rest or during light physical activity, X-ray signs of pulmonary congestion, a proven need for digoxin therapy following earlier withdrawal, or atrial fibrillation with a ventricular rate higher than 95 beats/min. A patient, who within two months presented signs of cardiac failure or an arrhythmia requiring digoxin, was considered to be in need of digoxin. Digoxin was withdrawn from a total of 141 patients, of whom 134 were examined after two months. According to our criteria, 108 (81%) of these 134 patients did not require digoxin treatment.

Age Factors↗
PubMed1977

Digoxin measurements in general practice.

1 As part of a prospective study on the use of digoxin in a general practice, plasma digoxin concentrations were measured in all patients receiving the drug. 2 A low mean plasma digoxin concentration was observed, suggesting a cautious approach to digitalization. 3 The correlation between plasma digoxin concentration and signs or symptoms commonly used in the assessment of digoxin effect was poor. 4 It was concluded that the measurement of plasma digoxin could be of assistance in a variety of clinical settings within a general practice.

Aged↗
PubMed1981

The early and late effects of digoxin treatment on the sodium transport, sodium content and Na+K+- ATPase or erythrocytes.

1 Erythrocyte sodium content, sodium transport (ouabain sensitive sodium flux Eos, and ouabain sensitive efflux rate constant ERCos) sodium, potassium activated ouabain sensitive adenosine triphosphatase (Na+K+ATPase) and plasma digoxin were measured in patients during acute digitalisation and in patients who were on long-term digoxin treatment. 2 In the six patients who were studied during digitalisation, the ERCos and Na+K+ATPase activity decreased and erythrocyte sodium content increased during days 2-4 treatment, but there was no change in Eos. 3 In 39 patients on long term digoxin therapy (2-119 months) the erythrocyte sodium content was normal, but the erythrocyte Na+K+ATPase activity was higher than the control group. When the results from these 39 patients were divided according to the duration of treatment it was found that the erythrocyte sodium content was higher in patients treated for 2-4 months than in patients treated for longer periods and the erythrocyte Na+K+ATPase activity increased with duration of treatment. In eight patients (duration of treatment greater than 29 months) in whom ERCos and Eos were measured, ERCos and Eos were higher than the control group. 4 The results suggest that the effects of digoxin on erythrocytes which occur during acute digoxin treatment do not persist in the long term. 5 The possible explanation for the higher ERCos, Eos and Na+K+ATPase activity in patients treated with digoxin for more than 2 months is discussed.

Aged↗
PubMed1983

The effect of digoxin on 86rubidium uptake by erythrocytes from mothers and babies.

1 The uptake of 86rubidium by erythrocytes from mothers and babies has been used as a model system to investigate possible differences in sensitivity to digoxin in the very young. 2 While total 86rubidium uptake was not significantly different between mothers and babies, the digoxin-sensitive proportion was higher in neonatal erythrocytes. Neonatal cells were less sensitive to digoxin, demonstrated by the requirement for a larger amount of digoxin to inhibit 86rubidium uptake and this was accompanied by an increase in numbers of specific erythrocyte binding sites for digoxin. 3 These results provide further evidence in support of the hypothesis of decreased sensitivity to digoxin in the very young.

Digoxin↗
PubMed1986

In vivo cation transport during short-term and long-term digoxin therapy.

We have studied the effects of digoxin on cation transport in vivo by measuring the changes in plasma and red cell rubidium concentrations following an oral load of rubidium chloride. In eight patients who had been taking digoxin for 7 to 10 days (mean plasma digoxin concentration 1.3 ng ml-1) the rise in plasma rubidium concentrations was enhanced and the rise in red cell rubidium concentrations was attenuated following the oral load of rubidium chloride, by comparison with the changes in well-matched controls. In contrast, the disposition of rubidium was not altered in 12 patients who had been taking digoxin for more than 3 months (mean plasma digoxin concentration 1.1 ng ml-1). These results suggest that the inhibitory effects of digoxin on cation transport are detectable in vivo during short-term therapy, but not during long-term therapy, and confirm our previous in vitro findings.

Adult↗
PubMed1991

Interaction between digoxin and indomethacin or ibuprofen.

To study a potential interaction between digoxin and two non-steroid anti-inflammatory drugs, indomethacin (50 mg three times daily) and ibuprofen (600 mg three times daily) were given for 10 days to 10 and 8 patients, respectively, on chronic digoxin treatment. Serum digoxin measured by fluorescence polarisation immunoassay increased significantly (P less than 0.05) during treatment with indomethacin from pre-treatment values of 0.73 +/- 0.34 nmol l-1 (mean +/- s.d.) to a mean value of 1.02 +/- 0.43 nmol l-1, while administration of ibuprofen did not change the steady state serum concentration of digoxin. The result demonstrates that some non-steroidal anti-inflammatory drugs such as indomethacin increase serum digoxin to levels high in the therapeutic range. This should be taken into consideration when co-administering other drugs known to increase the serum concentration of digoxin such as several antiarrhythmics.

Aged↗
PubMed1991

Minor effect of multiple dose omeprazole on the pharmacokinetics of digoxin after a single oral dose.

1. The influence of multiple dose administration of omeprazole on the pharmacokinetics of oral digoxin was studied in 10 healthy male volunteers. 2. In a randomized two-way crossover design a single dose of 1 mg digoxin was administered either alone (control) or on day 8 of an 11 day course of omeprazole 20 mg once daily. 3. Plasma digoxin concentrations were measured over 96 h after digoxin administration with a [125I]-r.i.a. method. 4. On average, Cmax and AUC values for digoxin were approximately 10% higher and tmax tended to be shorter during the administration of omeprazole, while the elimination rate constant was unaffected. 5. The increase in AUC(0,96 h) was statistically significant (P less than 0.05), but within the accepted range for bioequivalence. In two subjects the increase was approximately 30%. 6. It is concluded that co-treatment with omeprazole causes a minor increase in the absorption of oral digoxin. The magnitude of this effect is not considered to be clinically relevant for the majority of patients.

Administration, Oral↗
PubMed1995

The interaction of the calcium antagonist RO 40-5967 with digoxin.

1. The interaction of the newer calcium antagonist Ro 40-5967 with digoxin was investigated in 42 healthy subjects under steady state conditions. 2. After an adequate loading dose digoxin 0.375 mg once daily was given alone for 1 week. Afterwards three different doses (50, 100, 150 mg daily) of the calcium antagonist Ro 40-5967 were administered to three groups of 14 subjects each for 1 week concurrently with digoxin 0.375 mg daily. 3. Ro 40-5967 led to an increase of mean maximum digoxin plasma concentrations (Cmax) and AUC. For AUC this effect was significantly dose-dependent. 4. Increasing doses of the calcium antagonist led to a stepwise rise of the PQ-time in ECG. 5. A slight fall of heart rate was seen after a 7 day treatment of digoxin alone. This effect was more pronounced when Ro 40-5967 was added to the medication. No significant changes of stroke volume and blood pressure were noted. 6. In conclusion Ro 40-5967 led to a significant elevation of the plasma concentration-time curve (AUC) of digoxin. This effect was dose-dependent.

Administration, Oral↗
PubMed1987

Quinidine reduces biliary clearance of digoxin in man.

Quinidine is known to reduce the renal clearance of digoxin, but this effect does not completely explain the influence of quinidine on the total clearance of digoxin. We therefore studied the effect of quinidine administration on biliary clearance of digoxin in five patients with atrial fibrillation. Biliary clearance of digoxin under steady state conditions before and during treatment with quinidine was investigated using a duodenal-marker-perfusion technique. Quinidine caused an average 42% (range 21-65%, P less than 0.02) reduction of the measured biliary clearance of digoxin. We conclude that the biliary effect adds to the previously demonstrated inhibitory effect of quinidine on the renal clearance of digoxin and helps to explain the decrease in total clearance of the drug. This is the first demonstration in man of a pharmacokinetic drug interaction at the level of biliary excretion.

Aged↗
PubMed1989

Digoxin enhances the pressor response to aldosterone administration in conscious sheep.

1. This study examined the hypothesis that inhibition of Na,K ATPase with digoxin would enhance the pressor response to aldosterone infusion in conscious sheep. 2. While intravenous infusion of digoxin (10 micrograms/kg per day for 5 days) had no effect on blood pressure and aldosterone infusion (6 micrograms/kg per day for 5 days) increased blood pressure by 7 mmHg, combined infusion of digoxin and aldosterone increased blood pressure by 17 mmHg. 3. The metabolic effects of the combined digoxin and aldosterone infusion were similar to those for aldosterone alone, suggesting that digoxin did not enhance the mineralocorticoid action of aldosterone. 4. The results of this study suggest that changes in Na influx (aldosterone-dependent) and efflux (digoxin-dependent) are important in the genesis of aldosterone-induced hypertension.

Aldosterone↗
PubMed1988

Effects of oral prazosin on total plasma digoxin levels.

Prazosin and digoxin are frequently coadministered in clinical practice. To determine the effects of oral prazosin treatment on steady-state digoxin levels, 20 patients receiving a constant maintenance dose of digoxin, who had normal renal and liver functions and were not receiving any other treatment, were given 5 mg of prazosin for 3 days. Plasma digoxin levels were measured before, on days 1 and 3 of prazosin treatment, and after prazosin had been discontinued. It was found that prazosin significantly increased plasma digoxin levels. On discontinuation of prazosin digoxin levels returned to their previous values.

Administration, Oral↗
PubMed2002

Specific therapy of digoxin intoxication in dogs by hybrid kidney overexpressing multidrug resistance protein.

BACKGROUND: We have recently developed a unique hybrid artificial kidney, where the proximal tubular cell line, over-expressing multidrug resistance protein, MDR-1 (PCTL-MDR), was cultured on hollow fibers. While this module efficiently removed digoxin in vitro, its efficacy in vivo remained to be determined. METHODS: The system was scaled up by connecting 10 similar modules in parallel, with the MDR-1 (PCTL-MDR) overexpressed proximal tubular cell line cultured as in our previous study. The system was connected to dogs intoxicated with digoxin, a representative substrate of MDR-1. Blood was circulated for 90 minutes through the system. Arterial and venous blood concentrations of digoxin and inulin were monitored. Complete blood cell count and granulocyte elastase were measured before and at the end of the study. RESULTS: By using the system with PCTL-MDR, the arterial digoxin concentration was dramatically decreased from 2.89 +/- 0.10 to 0.92 +/- 0.11 ng/mL, but not by the system with PCTL alone. The clearance was 22.4 +/- 2.1 and 1.5 +/- 0.2 mL/min for the PCTL-MDR and PCTL equipment, respectively. Inulin was not transported in either system. White blood cell and platelet counts were slightly reduced by the treatment while hematocrit was unchanged; the granulocyte elastase concentration was slightly increased. CONCLUSION: These data suggest that our new type of hybrid kidney can selectively remove digoxin sufficiently to reduce its systemic blood concentration in dogs with digoxin intoxication. Taking previous studies into consideration, this system may be a more powerful tool for the treatment of intoxication.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1996

Effect of digoxin on the ventricular rate variability during paroxysmal atrial fibrillation.

This study investigated whether the irregularity of ventricular cycle length during atrial fibrillation (AF) is affected by digoxin. Patients (n = 41) with paroxysmal AF enrolled in a randomized crossover comparison of digoxin and placebo underwent 24-hour ambulatory monitoring during each treatment. Tapes containing AF episodes lasting at least 2 minutes were selected (24 recordings on placebo and 17 on digoxin). The mean (mRR) and standard deviation (SDRR) of RR intervals was calculated for each 30-second segment of AF. The resulting SDRR values were clustered according to bins of mRR values ranging from 350-650 ms in 25-ms steps. In each bin, the SDRR values of all placebo and all digoxin recordings were statistically compared for the top 5, 10, and 15 percentiles of each bin which represented the extremes of ventricular cycle length irregularity during AF. There were no significant differences between the total data of SDRR values in individual bins of mRR. However, the top 5, 10, and 15 percentiles of SDRR values corresponding to mRR values from 350-550 ms were significantly reduced by digoxin (P < 0.0001). The study concludes that although digoxin does not influence the mean variability of RR cycles during AF paroxysms, it suppresses episodes in which a fast ventricular response is associated with extreme variability of RR periods.

Anti-Arrhythmia Agents↗
PubMed1979

Effects of digoxin on isolated human peripheral arteries and veins.

In isolated human crural arteries and veins, digoxin induced slowly developing, long-lasting contractions. These contractions were not diminished by alpha-adrenoceptor blockade or by washing, but were abolished by the calcium antagonist nifedipine. In the presence of digoxin, the maximum contractile responses to noradrenaline (18 microM) and potassium (127 mM) markedly increased, and the glycoside shifted the noradrenaline concentration-response curve to the left. Immersion of vein preparations in calcium-free medium for 30 min. abolished the digoxin contraction, whereas responses could still be elicited by potassium and noradrenaline. A change of the extracellular potassium concentration from 4.6 to 6.9 and 9.2 mM caused relaxation, and a further increase to 13.8 mM contracted the preparations. After pretreatment with digoxin (1 micronM), a potassium change from 4.6 to 1.15 mM caused relaxation and all concentrations exceeding 4.6 mM produced contraction. It is concluded that digoxin has a direct contractile effect on isolated human crural vessels, and that this effect is dependent on the extracellular calcium concentration. In the presence of the glycoside, the responses to noradrenaline and potassium are potentiated. Vascular responses to changes in extracellular potassium concentration are influenced by digoxin.

Adolescent↗
PubMed1985

Modification of the inotropic effect of digoxin by diazepam in rat left atria.

There is a pharmacokinetic interaction between digoxin and diazepam that increases the elimination half-life of digoxin. It may be due to a reduction of digoxin tissue concentrations and to an enhanced effect of diazepam on digoxin binding to plasma albumin. Diazepam (10(-5) M) also induces a positive inotropic effect in guinea-pig isolated atria. In a study of a possible pharmacodynamic interaction between both drugs, the inotropic response to digoxin has been examined in rat isolated atria in the presence of diazepam. The atria were kept in Tyrode at 37 degrees C, bubbled with 95% O2 and 5% CO2 and electrically stimulated at twice the threshold voltage. The results indicate that diazepam induces an inotropic effect at 10(-5) M (P less than 0.05) and reduces (P less than 0.05) at 10(-9), 10(-7) and 10(-5) M the inotropic response to digoxin (10(-5) M).

Animals↗
PubMed1987

Central dopamine receptors and their role in digoxin-induced cardiotoxicity in the dog.

The role of the dopaminergic system in digoxin-induced cardiotoxicity has been examined. Specific dopaminergic agonists and antagonists were administered into the ventriculocisternal system of pentobarbitone-anaesthetized dogs before systemic administration of digoxin. Pretreatment with apomorphine, a specific dopamine agonist, did not significantly alter the arrhythmogenic or lethal doses of digoxin. However, the digoxin-induce increase in CSF noradrenaline was decreased significantly in apomorphine-pretreated animals. Pretreatment with pimozide, a specific dopamine antagonist, significantly decreased the arrhythmogenic dose of digoxin but did not alter the lethal dose. As with apomorphine, pimozide-pretreated animals accumulated significantly less noradrenaline in CSF compared with control dogs. These results suggest that dopamine receptors are not directly related to the cardiotoxic actions of digoxin. However, dopaminergic receptors may influence the balance of central catecholaminergic systems that influence the peripheral cardiovascular system.

Animals↗
PubMed2006

Effect of goldenseal (Hydrastis canadensis) and kava kava (Piper methysticum) supplementation on digoxin pharmacokinetics in humans.

Phytochemical-mediated modulation of P-glycoprotein (P-gp) and other drug transporters may give rise to many herb-drug interactions. Serial plasma concentration-time profiles of the P-gp substrate, digoxin, were used to determine whether supplementation with goldenseal or kava kava modified P-gp activity in vivo. Twenty healthy volunteers were randomly assigned to receive a standardized goldenseal (3210 mg daily) or kava kava (1227 mg daily) supplement for 14 days, followed by a 30-day washout period. Subjects were also randomized to receive rifampin (600 mg daily, 7 days) and clarithromycin (1000 mg daily, 7 days) as positive controls for P-gp induction and inhibition, respectively. Digoxin (Lanoxin, 0.5 mg) was administered p.o. before and at the end of each supplementation and control period. Serial digoxin plasma concentrations were obtained over 24 h and analyzed by chemiluminescent immunoassay. Comparisons of area under the curve (AUC)((0-3)), AUC((0-24)), C(max,) CL/F, and elimination half-life were used to assess the effects of goldenseal, kava kava, rifampin, and clarithromycin on digoxin pharmacokinetics. Rifampin produced significant reductions (p < 0.01) in AUC((0-3)), AUC((0-24)), CL/F, t(1/2), and C(max), whereas clarithromycin increased these parameters significantly (p < 0.01). With the exception of goldenseal's effect on C(max) (14% increase), no statistically significant effects on digoxin pharmacokinetics were observed following supplementation with either goldenseal or kava kava. When compared with rifampin and clarithromycin, supplementation with these specific formulations of goldenseal or kava kava did not appear to affect digoxin pharmacokinetics, suggesting that these supplements are not potent modulators of P-gp in vivo.

Adult↗