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PubMed1984

Effect of metoclopramide on digoxin absorption from tablets and capsules.

The effect of metoclopramide, a drug that increases gut motility, on the consistency of digoxin absorption was examined in 16 healthy men. Each received the following four single-dose digoxin treatments in complete crossover fashion: two 0.25-mg digoxin tablets, alone, and two 0.2-mg digoxin capsules with metoclopramide. Mean serum AUCs over 24 hr (AUC-24) and cumulative urinary digoxin excretion over 48 hr (CUE-48) were of the same order for the tablets and capsules alone treatments. Metoclopramide reduced the mean AUC-24 for tablets from 12.26 +/- 2.70 to 9.38 +/- 3.78 ng X hr/ml (P less than 0.001) and the CUE-48 from 119.0 +/- 22.4 to 97.6 +/- 22.2 micrograms (P less than 0.01). There were no significant differences in mean AUC-24 (12.94 +/- 3.16 and 13.45 +/- 2.33 ng X hr/ml) and mean CUE-48 (117.8 +/- 23.4 and 109.7 +/- 25.0 micrograms) when capsules alone were compared to capsules with metoclopramide. Metoclopramide reduced the time to reach peak concentration for both digoxin dosage forms. The effect of metoclopramide on digoxin absorption is minimized by administration of digoxin in capsules.

Absorption↗
PubMed1988

Comparative effects of verapamil and isradipine on steady-state digoxin kinetics.

The effects on the steady-state digoxin pharmacokinetics of verapamil (240 mg/day) and a new dihydropyridine calcium channel blocker, isradipine (15 mg/day), were compared. Nineteen healthy white men, aged 23 to 40 years, ingested 0.25 mg digoxin tablets every 12 hours for two consecutive periods of 2 weeks. Each subject also received one of the calcium channel blockers during one of these periods, with agent and sequence randomized. Analyst-blind RIA serum digoxin determinations demonstrated that the nine subjects who received isradipine, 5 mg t.i.d., had a small increment in peak digoxin level from 2.3 +/- 0.6 to 2.9 +/- 0.7 ng/ml (p less than 0.05) but no significant change in steady-state level or AUC over 12 hours. By contrast, the 10 subjects who received verapamil, 80 mg t.i.d., showed significant increases in steady-state (0.9 +/- 0.1 to 1.3 +/- 0.2 ng/ml; p less than 0.001) and peak serum digoxin concentrations (2.5 +/- 0.7 to 3.6 +/- 0.8 ng/ml; p less than 0.001) and in AUC (15.7 +/- 1.7 to 23.6 +/- 2.9 ng . hr/ml; p less than 0.001). Neither calcium channel blocker reduced renal digoxin clearance. Verapamil increases digoxin levels without affecting renal clearance. Isradipine has no clinically important interaction with digoxin.

Adult↗
PubMed1993

Disposition of digoxin immune Fab in patients with kidney failure.

Digoxin and digoxin immune Fab, its antidote, are eliminated renally. However, the disposition of Fab in severe kidney disease is poorly described. Therefore, the disposition of Fab and its relationship to total and free digoxin were studied in five digoxin-toxic patients with end-stage renal disease (n = 4) or severe renal dysfunction (n = 1) with a mean (+/- SD) serum creatinine of 5.9 +/- 1.2 mg/dl (four patients were receiving long-term hemodialysis). Serum was drawn after a clinically neutralizing Fab dose (80 to 160 mg) every 12 to 24 hours for 204 to 327 hours. Fab concentrations were assessed by radioimmunoassay, whereas total digoxin concentrations were assessed with a modified radioimmunoassay or fluorescence polarization immunoassay. The concentration-time profile of Fab appeared to be similar to the concentration-time profile of total digoxin. The mean (+/- SD) half-lives of the alpha and beta disposition phases of Fab were 13 +/- 5 hours and 96 +/- 31 hours, respectively, which were similar to the alpha and beta parameter estimates of total digoxin (14 +/- 4 and 123 +/- 16 hours, respectively). Steady-state volume of distribution and systemic clearance of Fab were 0.29 +/- 0.11 L/kg and 0.057 +/- 0.022 ml/min/kg, respectively. Thus, in comparison to values reported in patients with normal renal function, the elimination of Fab and total digoxin are markedly delayed in patients with end-stage renal disease, which may necessitate prolonged clinical monitoring.

Aged↗
PubMed1997

Pharmacokinetic and pharmacodynamic interaction trial after repeated oral doses of imidapril and digoxin in healthy volunteers.

AIMS: To investigate the potential pharmacokinetic and pharmacodynamic interaction between imidapril and digoxin. METHODS: AUC, Cmax and t(max) of imidapril, imidaprilat and digoxin were calculated and evaluated in a randomized, doubleblind three-period cross-over design in 12 healthy volunteers after 8 days treatment with the following combinations: digoxin 0.25 mg day(-1) + placebo (D + P); imidapril 10 mg day(-1) + placebo (I + P); imidapril 10 mg day)(-1) + digoxin 0.25 mg day(-1) (I + D). RESULTS: Mean AUC (0, 24 h) of digoxin was 10.4 (+/- 4.9 s.d.) ng ml(-1) h (D + P) and 10.7 (+/- 3.9 s.d.) ng ml(-1) h (I + D), respectively (90%-confidence intervals [CI] for the ratio of (D + P) and (I + D): 0.91-1.27, point estimator [PE]: 1.06). Mean AUC (0, 24 h) of imidapril was 133 (+/- 86 s.d.) ng ml(-1) h (I + P) and 108 (+/- 52 s.d.) ng ml(-1) h (I + D), respectively (90%-CI: 0.76-0.94, PE 0.85). AUC (0, 24 h) of imidaprilat was 215 (+/- 91 s.d.) ng ml(-1) h (I + P) and 194 (+/- 54 s.d.) ng ml(-1) h (I + D), respectively (90%-CI: 0.80-1.08, PE 0.93). Cmax was 19.9 (+/- 8.7 s.d.) ng ml(-1) (I + P) and 15.9 (+/- 5.3 s.d.) ng ml(-1) (I + D) (90%-CI: 0.67-1.00, PE 0.82). The results indicate a slight reduction of imidapril and imidaprilat plasma levels when coadministered with digoxin without any effect on digoxin plasma levels. Maximal ACE-inhibition was 79% (I + P) and 67% (I + D). CONCLUSIONS: Grouped data analysis of imidaprilat plasma levels vs ACE-activity showed that for maximal inhibition of plasma ACE activity, imidaprilat plasma levels should exceed 10 ng ml(-1). Under digoxin and imidapril, more plasma concentrations of imidaprilat were seen under this level as after imidapril alone, this reduces the integral of the ACE-inhibition/time curves by about 20 to 30%.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Lack of effect of eprosartan on the single dose pharmacokinetics of orally administered digoxin in healthy male volunteers.

AIMS: To study the effect of eprosartan, a nonbiphenyl tetrazole angiotensin II receptor antagonist, on digoxin pharmacokinetics in a randomized, open-label, two period, period balanced crossover study in 12 healthy men. METHODS: Each subject received a single 0.6 mg oral dose of digoxin (Lanoxicaps 0.2 mg/capsule, Glaxo Wellcome) alone or following 4 days of dosing with eprosartan 200 mg orally every 12 h. Each study period was separated by a 14 day washout interval. Serial blood samples were obtained for up to 96 h after each digoxin dose for determination of digoxin pharmacokinetics. The effect of eprosartan on digoxin pharmacokinetics was assessed through an equivalence-type approach using AUC(0, t') as the primary endpoint. RESULTS: For AUC(0, t'), the ratio of digoxin+eprosartan: digoxin alone was 0.99 with a 90% confidence interval (CI) of [0.90, 1.09]. For Cmax, the ratio was 1.00 with a 90% CI of [0.86, 1.17]. tmax was similar for both regimens. Both regimens were safe and well tolerated. CONCLUSIONS: Based on AUC and Cmax data, it can be concluded that eprosartan has no effect on the pharmacokinetics of a single oral dose of digoxin.

Acrylates↗
PubMed2002

Absence of a pharmacokinetic interaction between digoxin and levofloxacin.

BACKGROUND: Levofloxacin, a broad-spectrum fluoroquinolone, may enhance digoxin bioavailability by eliminating intestinal flora that metabolize digoxin. Moreover, levofloxacin, which is eliminated primarily by glomerular filtration and active tubular secretion, may alter the elimination rate of digoxin. Because of the narrow therapeutic index of digoxin, it is important to evaluate the potential for interaction with levofloxacin when administered concomitantly. METHODS: This was a placebo-controlled, randomized, double-blind, two-phase crossover study. Twelve healthy subjects (six males and six females) received 500 mg twice/day oral doses of levofloxacin or placebo for 6 days and a single oral dose of 0.4 mg digoxin on the morning of study day 5 along with levofloxacin or placebo. RESULTS: There was no significant effect of levofloxacin on the pharmacokinetics (Cmax, AUC, and other disposition parameters) of oral digoxin. Steady-state levofloxacin absorption and disposition kinetics were also similar in the presence or absence of digoxin. CONCLUSIONS: Results of this study suggest that an important pharmacokinetic interaction between levofloxacin and digoxin is unlikely to occur when administered concomitantly.

Administration, Oral↗
PubMedDate not supplied

Comparison of digoxin versus low-dose amiodarone for ventricular rate control in patients with chronic atrial fibrillation.

1. Rapid ventricular rate (VR) and rhythm irregularity during atrial fibrillation (AF) impair cardiac performance. Although digoxin has been widely used in patients with AF, its efficacy for the control of VR and rhythm irregularity is unsatisfactory. Whether low-dose amiodarone is more effective remains unclear. 2. We randomized 16 patients (13 male, three female; mean (+/-SD) age 63 +/- 9 years) with chronic AF to receive either digoxin or amiodarone for 24 weeks. At baseline and at 12 and 24 weeks follow up, Holter monitor recording and cardiopulmonary exercise test were performed to assess VR and rhythm irregularity control and exercise capacity. 3. Seven and nine patients received digoxin and amiodarone, respectively. After 12 and 24 weeks treatment, both digoxin and amiodarone significantly decreased the mean ambulatory VR and the VR during peak exercise compared with baseline (all P < 0.05). At 24 weeks, there were no significant differences between digoxin and amiodarone in the percentage reduction in VR during ambulatory (27 +/- 13 vs. 25 +/- 12%, respectively; P = 0.8) and peak exercise (13 +/- 12 vs. 12 +/- 10%%, respectively; P = 0.6). 4. The rhythm irregularity, as measured by SD of RR intervals and the root mean square of the SD of RR intervals, and the exercise capacity, as measured by exercise workload, maximal oxygen consumption (VO2), minute ventilation, ventilatory equivalent and oxygen pulse, were not significantly changed after treatment with digoxin or amiodarone (all P > 0.05). 5. Quality of life, determined by SF-36 questionnaire, and AF symptomatology, as measured by the AF Symptom Checklist, were also not significantly changed after treatment with digoxin or amiodarone (all P > 0.05). 6. In conclusion, digoxin and low-dose amiodarone had similar efficacy in the control of VR during ambulatory activity and exercise. However, both were less efficacious during exercise and did not significantly affect rhythm irregularity, exercise capacity, quality of life and AF symptomatology in patients with chronic AF.

Aged↗
PubMed1999

Pharmacokinetic interaction of digoxin with an herbal extract from St John's wort (Hypericum perforatum).

OBJECTIVE: Extracts of St John's wort (Hypericum perforatum) are widely used in the treatment of depression, often as an over-the-counter drug. In contrast to its frequent use, knowledge about the pharmacokinetics of ingredients and drug interactions of St John's wort is poor. We studied the interaction between hypericum extract LI160 and digoxin. METHODS: The pharmacokinetics of digoxin were investigated in a single-blind, placebo-controlled parallel study. After the achievement of steady state for digoxin on day 5, healthy volunteers received digoxin (0.25 mg/d) either with placebo (n = 12) or with 900 mg/d LI160 (n = 13) for another 10 days. Digoxin concentration profiles on day 5 were compared with day 6 (single-dose interaction) and day 15 (tenth day of co-medication). RESULTS: There was a highly significant combined-day-and-group effect for digoxin area under the plasma concentration-time curve [AUC(0-24); P = .0001], peak concentration in plasma (Cmax; P = .0001), and plasma drug concentration at the end of a dosing interval (P = .0003) by two-way ANOVA. No statistically significant change was observed after the first dose of hypericum extract [AUC(0-24) at day 6 of 18.1+/-2.9 microg x h/L and 17.7+/-3.0 microg x h/L, mean +/- SD for placebo and hypericum group, respectively]. However, 10 days of treatment with hypericum extract resulted in a decrease of digoxin AUC(0-24) by 25% (day 15, 17.2+/-4.0 microg x h/L and 12.9+/-2.3 microg x h/L; P = .0035). Furthermore, comparison with the parallel placebo group after multiple dosing showed a reduction in trough concentrations and Cmax of 33% (P = .0023) and 26% (P = .0095), respectively. The effect became increasingly pronounced until the tenth day of co-medication. CONCLUSION: As with grapefruit juice, a food product, physicians should also be aware of potential drug-herb interactions. The interaction of St John's wort extract with digoxin kinetics was time dependent. The mechanism involved may be induction of the P-glycoprotein drug transporter.

Adult↗
PubMed2003

The effect of digoxin on the quality of life in patients with heart failure.

BACKGROUND: The Digitalis Investigation Group (DIG) trial was a randomized double-blind placebo-controlled study that examined the effect of digoxin on mortality in 7,788 patients with heart failure and sinus rhythm. A prespecified substudy evaluated the effect of digoxin therapy on health-related quality of life (HQOL) in a subset of these patients. METHODS: Patients in the DIG trial had clinical heart failure and were randomized to either digoxin or placebo in addition to their baseline diuretic and angiotensin-converting enzyme therapy (n = 7,788). The patients in this substudy had HQOL measured using a self-administered questionnaire employing scales that measured general health, physical functioning, depression, anger, anxiety, life satisfaction, and disease specific measures. A subjective assessment by the investigator and a 6-minute walk test evaluated functional status. HQOL was measured at baseline and at the 4- and 12-month follow-up visits. RESULTS: The baseline characteristics of the patients in the quality of life substudy (n = 589) were comparable to the remaining patients in the study (n = 7,199) by age and other clinical measures, including history of prior myocardial infarction or etiology of heart failure; heart failure was of shorter duration and the ejection fraction was slightly better than in the main trial. Within the substudy, patients receiving digoxin (n = 298) or placebo (n = 291) were also similar in baseline characteristics. There was no statistically significant difference in any HQOL measure between the digoxin and the placebo groups at baseline. At the 4-month visit, only perceived health was improved in the digoxin group. At 12 months, there was no statistically significant difference in perceived health, physical functioning, Minnesota Living with Heart Failure, depression, anxiety, anger, Ladder of Life, or the 6-minute walk between the digoxin and placebo groups. CONCLUSION: In this subset of the DIG population, digoxin therapy had no effect on the HQOL in patients with heart failure in sinus rhythm.

Aged↗
PubMed1979

[Interaction of quinidine and digoxin in humans (author's transl)].

After full digitalisation, 11 healthy subjects received 0.375 mg digoxin daily as maintenance dose. Under steady-state conditions and determination of serum concentration and renal clearance of digoxin, they were then given 500 or 1000 mg quinidine daily in addition to the digoxin. While serum concentration of digoxin rose significantly from 0.75 +/- 0.2 ng/ml after one week on 500 mg quinidine, and to 1.8 +/- 0.6 ng/ml after 1000 mg of quinidine, renal digoxin clearance fell from 186.2 +/- 67.4 to 125.4 +/- 61.8 ml/min after 500 mg of quinidine. Raising quinidine dosage to 1000 mg daily caused no further digoxin clearance reduction. During the total experimental period endogenous creatinine clearance remained unchanged. The results indicate that the rise in serum digoxin concentration on simultaneous quinidine administration is largely due to reduction in renal digoxin clearance. A clinical observation confirms the considerable practical importance of this interaction.

Digoxin↗
PubMed2000

Study on the interaction of the dopamine agonist alpha-dihydroergocryptine with the pharmacokinetics of digoxin.

AIM: The study was carried out to explore the potential for pharmacokinetic interaction of a single oral dose of alpha-dihydroergocryptine (CAS 14271-05-7, DHEC, Almirid) with digoxin. METHODS: The serum pharmacokinetics of digoxin were analysed after the administration of single oral doses of 0.5 mg digoxin administered either alone or concomitantly with 20 mg DHEC according to a randomised, non-blinded, two-period cross-over design, with study periods 2 weeks apart. Twelve healthy male subjects, 23 to 39 years of age were enrolled and were investigated in accordance with the protocol. Venous blood was sampled up to 48 h after dosing. Concentrations of digoxin in serum were determined by a competitive radioimmunoassay. RESULTS: The mean Cmax were 1.97 +/- 0.87 (after a median tmax of 1 h) and 2.05 +/- 0.95 ng/ml (after a median tmax of 0.83 h) after the administration of digoxin with (test) and without (reference) concomitant DHEC, respectively; the corresponding estimated treatment ratio for test: reference was 0.939, 95% CI: 0.781 to 1.129. The mean AUC(0-48) were 13.6 +/- 5.0 ng.h/ml and 13.3 +/- 4.7 ng.h/ml for the test and reference treatment, respectively; the corresponding estimated treatment ratio for test: reference was 1.011, 95% CI: 0.866 to 1.142. In addition, no clinically significant changes were observed by ECG monitoring. The tolerability of digoxin alone was good, significantly more adverse events occurred when co-administered with DHEC; these corresponded with the known adverse reaction profile and were of moderate intensity. No premature study termination was thus necessary. CONCLUSION: The present study did not demonstrate clinically relevant interaction of a single dose of DHEC on the pharmacokinetics of digoxin. On the basis of these observations there is no indication for an a priori adjustment of the dose of digoxin when concomitant treatment with DHEC is initiated.

Adolescent↗
PubMedDate not supplied

[Maternal and fetal digoxin level in fetofetal transfusion syndrome (FFTS)].

BACKGROUND: Even though invasive intrauterine techniques for the treatment of TTTS such as punction of amniotic fluid and laser coagulation of placental vascular anastomoses are established methods in specialized centers, invasive methods are not always sufficiently successful. In conservative treatment of TTTS oral or intravenous maternal digoxin therapy in order to improve fetal cardiac insufficiency in combination with or after failure of invasive techniques is an useful method. PATIENTS AND METHODS: We investigated 12 TTTS pregnancies and 4 singleton pregnancies, which had been treated by maternal digoxin treatment for TTTS or arrhythmias, respectively. At birth, which was performed by means of caesarian section, venous cord blood samples of the newborns and venous maternal blood samples were collected, centrifugated and stored at minus 20 degrees C. Digoxin determinations were performed by radioimmunoassay. RESULTS: Fetal digoxin levels varied between 0.38 and 1.73 ng/ml, maternal levels ranged from 0.97 to 3.23 ng/ml. The fetomaternal digoxin gradient reached a mean of 0.56 (range 0.35 to 1.09). Donator and acceptor gradients were comparable and increased with birth weight or gestational week, respectively. CONCLUSIONS: In cases of pregnancies with TTTS a relatively high maternal digoxin level is necessary, especially during early gestational weeks, in order to reach therapeutical levels in the fetal circulation. Too low dosages might be responsible for unfavourable results in digoxin treatment of TTTS. Whether the maturation of placental villi during gestation could be the reason for increasing digoxin gradients requires further investigations.

Administration, Oral↗
PubMed1979

Digoxin-quinidine interaction Pharmacokinetic evaluation.

Several recent reports have shown that plasma concentrations of digoxin increase when quinidine is administered along with digoxin; the present study was designed to explore the pharmacokinetics of this digoxin-quinidine interaction in six subjects. The elimination half-life of digoxin, although variable, did not change appreciably (42 vs. 44 hours) when quinidine was administered. Other pharmacokinetic values were substantially reduced in the presence of quinidine: total body clearance (from 3.08 to 1.96 ml per minute per kilogram), renal clearance (from 1.64 to 1.09 ml per minute per kilogram) and volume of distribution (from 10.87 to 7.35 liters per kilogram). The results may be explained by the displacement of digoxin from binding sites in tissue by quinidine, causing a rise in the plasma concentration of digoxin. The reduction in renal clearance of digoxin may result also from inhibition of renal secretion of digoxin by quinidine.

Digoxin↗
PubMed1992

The use of digoxin-specific Fab fragments for severe digitalis intoxication in children.

BACKGROUND: Because life-threatening digitalis intoxication is unusual in children, treatment with digoxin-specific-antibody Fab fragments (Fab) has rarely been reported. We describe the efficacy of Fab in the treatment of children with severe digitalis intoxication. METHODS: Twenty-nine children with intoxication due to digoxin (28) or digitoxin (1) received Fab at 21 participating hospitals between 1974 and 1986. Data were gathered about the patients' medical illnesses, doses and serum concentrations of digitalis, responses to Fab therapy, and outcomes. RESULTS: In the infants and young children with acute digoxin intoxication, the digoxin doses ranged from 0.30 to 0.96 mg per kilogram of body weight; two adolescents had severe intoxication after doses of only 0.20 and 0.26 mg per kilogram. The serum digoxin concentrations ranged from 3.0 to greater than 100 ng per milliliter (mean, 13.8). Atrioventricular block (present in 22 patients [76 percent]) was the most common sign of toxicity. All the patients in this series had severe disturbances of cardiac rhythm, hyperkalemia (mean serum potassium concentration, 5.4 mmol per liter), or both. In 27 patients (93 percent), digitalis toxicity resolved after the administration of Fab. Of the 19 patients for whom data were available on the timing of the response to Fab, 15 responded within 180 minutes. Three patients required retreatment with Fab. Seven died of complications unrelated to the administration of Fab. CONCLUSIONS: We recommend that Fab be used in the treatment of digitalis poisoning in infants and young children who have ingested greater than or equal to 0.3 mg of digoxin per kilogram, who have underlying heart disease, or who have a serum digoxin concentration of greater than or equal to 6.4 nmol per liter (greater than or equal to 5.0 ng per milliliter) in the elimination phase; and who also have a life-threatening arrhythmia, hemodynamic instability, hyperkalemia, or rapidly progressive toxicity. Adolescents, who are more sensitive to the toxic effects of digoxin than younger children, may require treatment with Fab after ingesting lower doses.

Acute Disease↗
PubMed1983

Digoxin kinetics in the elderly.

Digoxin elimination phase kinetics have been studied in 24 hospital in-patients (mean age 79 years), six of whom showed no evidence of digoxin toxicity. The others, with suspected toxicity, have been grouped according to the nature of the drug effects observed. Renal function, digoxin elimination half-life, apparent volume of digoxin distribution, and notional body content of digoxin have been compared between the groups. Apart from two hyperthyroid patients, the volumes of distribution averaged 6.1 1/kg. Toxic patients tended to have lower creatinine clearances, longer digoxin half-lives, and higher body contents of digoxin than the nontoxic, but the highest body contents were found in those with systemic toxicity. Thyrotoxicosis increases the apparent volume of digoxin distribution in the elderly.

Aged↗
PubMed1976

Steady-state kinetics of digoxin in the elderly.

Renal clearance of digoxin and creatinine was determined simultaneously on 30 occasions in 28 elderly in-patients on maintenance digoxin therapy. The mean ratio of digoxin to creatinine clearance was 1.04 (+/- S.E.M. 0.08). Multiple 24-hour urinary excretions of digoxin were measured in 10 patients on digoxin on a dose of 0.25 mg/day, four on 0.125 mg/day, and six on 0.0625 mg/day. Mean urinary excretion was 42% of dose per day. Calculated "net biliary clearance" averaged 18 ml/min. Knowledge of the magnitude of renal and net biliary clearance, together with assumed values for fractional absorption allows a relationship between serum digoxin levels and creatinine clearance to be calculated for each dose level. There was reasonable agreement between observed and expected serum digoxin levels in 41 elderly patients in whom creatinine clearance was measured, and in 106 in whom glomerular filtration rate was estimated from serum urea and creatinine concentrations. Quantitation of the kinetics of digoxin in the elderly can make maintenance therapy more rational and therefore safer and more effectove.

Age Factors↗
PubMed1993

Interaction of itraconazole and digoxin.

A 69-year-old man who had been taking digoxin for 2.5 years developed an elevated serum concentration of digoxin in association with digoxin toxicity (characterized by nausea and vomiting) 9 days after the addition of itraconazole to his regimen for the treatment of sternal osteomyelitis. Coadministration of itraconazole resulted in a statistically significant increase in the half-life of digoxin that necessitated a reduction of the digoxin dose by almost 60%. We thus recommend that patients receiving itraconazole and digoxin concomitantly have serum levels of digoxin monitored frequently. In addition, these patients should be carefully questioned about nonspecific gastrointestinal symptoms, which may indicate early digoxin toxicity.

Aged↗
PubMed1981

Effects of hypoxia on myocardial digoxin uptake and levels of plasma catecholamines in anaesthetised dogs.

The effect of hypoxia on digoxin pharmacokinetics, myocardial digoxin uptake and levels of plasma catecholamines in dogs was studied to clarify the mechanism of enhanced sensitivity to digitalis in hypoxia. Sixteen mongrel dogs were anaesthetised and artificially respired; eight with room air, eight with 8% oxygen in nitrogen, and digoxin (0.05 mg . kg-1) was intravenously given to each dog. There was no difference between hypoxic and non-hypoxic dogs in pharmacokinetic curves of digoxin. The level of myocardial digoxin in hypoxic dogs was significantly lower than that in non-hypoxic dogs. The level of plasma adrenaline in hypoxic dogs was significantly higher than that in non-hypoxic dogs (P less than 0.01). These data suggest that enhanced sensitivity to digoxin in hypoxia may be attributable not to abnormal digoxin pharmacokinetics or increased myocardial digoxin uptake but partly to higher levels of plasma catecholamines.

Animals↗