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PubMed1989

Absorption of digoxin from tablets and capsules in subjects with malabsorption syndromes.

The relative steady-state bioavailability of two oral digoxin dosage forms was studied in 17 subjects with malabsorption syndromes. Male subjects received the following treatments in randomized crossover fashion for 14 days: three 0.125-mg digoxin tablets or three 0.1-mg digoxin capsules once daily. Female subjects received digoxin on the same schedule but at two-thirds the dose. Serum and urine samples were collected and analyzed for digoxin by radioimmunoassay, and treatments were compared by evaluating pharmacokinetic parameters. The mean area under the serum concentration versus time curve for tablets (28.1 h.nmol/L [21.9 h.ng/mL]) was smaller (p less than 0.03) than that for capsules (31.1 h.nmol/L [24.3 h.ng/mL]), and the mean maximum serum digoxin concentration for tablets (2.9 nmol/L [2.3 ng/mL]) was lower (p less than 0.02) than that for capsules (4.0 nmol/L [3.1 ng/mL]). There was no difference in cumulative urinary excretion of digoxin between the two treatments. In contrast to previous reports, we observed that digoxin from Lanoxin Tablets appears to be well absorbed in subjects with malabsorption. Nevertheless, these subjects absorbed digoxin from capsules better than from tablets, with the greatest differences occurring in subjects without a colon and in those subjects with the lowest serum carotene concentrations.

Adult↗
PubMedDate not supplied

Concomitant digoxin toxicity and warfarin interaction in a patient receiving clarithromycin.

OBJECTIVE: To report a case of a clarithromycin-associated warfarin interaction and digoxin toxicity in a patient. CASE SUMMARY: A 72-year-old white woman with chronic atrial fibrillation receiving long-standing therapy with digoxin 0.25 mg/d and warfarin 22.5 mg/wk was prescribed clarithromycin 500 mg three times daily for eradication of Helicobacter pylori. The patient presented to the emergency department with gastrointestinal symptoms, weakness, dizziness, and visual changes 12 days after initiation of clarithromycin. Laboratory results revealed a serum digoxin concentration of 4.6 ng/mL (normal 1.0-2.6) and an international normalized ratio of 7.3 (2.0-3.0). Digoxin, warfarin, and clarithromycin were discontinued and the patient was admitted to the hospital for treatment to resolve the symptoms and to return laboratory values to a safe range. Reduced dosages of digoxin (0.125 mg/d) and warfarin (17.5 mg/wk) were restarted on day 7 of hospitalization. The patient was discharged on day 11 in good condition. DISCUSSION: Several reports of clarithromycin-induced drug interactions with digoxin and with warfarin have been published. Previously, case reports of macrolide-associated interactions mainly involved erythromycin, but more recently have implicated clarithromycin. The interaction between clarithromycin and warfarin is thought to occur from an inhibition of the cytochrome P450 drug metabolizing system. Clarithromycin is thought to cause digoxin toxicity by an alteration of the digoxin-metabolizing gut flora, thereby causing an increase in the digoxin concentration in susceptible individuals. Drug interactions can occur by different mechanisms in the same patient. CONCLUSIONS: Potential drug interactions can occur between commonly prescribed medications. It is important to monitor patients for symptoms and alterations in laboratory values to prevent not only serious complications, but also unnecessary hospitalizations.

Aged↗
PubMed2006

The safety of digoxin as a pharmacological treatment of atrial fibrillation.

Digoxin has traditionally been the drug of choice for ventricular rate control in patients with chronic atrial fibrillation (AF), with or without heart failure (HF) with systolic dysfunction. In patients with permanent AF, digoxin monotherapy is ineffective to control ventricular rate during exercise, but the combination of digoxin with a beta-blocker or a non-dihydropyridine calcium channel antagonist can control heart rate both at rest and during exercise. Only a few randomised, controlled studies have evaluated the adverse effects of digoxin in patients with AF in a systematic way and side effects requiring drug withdrawal have rarely been reported. When reported, the most frequent adverse effects were cardiac arrhythmias (ventricular arrhythmias, AV block of varying degrees and sinus pauses). This evidence suggested that, in contrast to other antiarrhythmic drugs, digoxin is a safe drug in patients with AF. However, this safety profile can be erroneous due to the short follow-up of the studies and patient selection. Because patients with HF have been excluded in most studies, the safety profile of digoxin in this population has not been directly addressed. Early recognition that an arrhythmia is related to digoxin intoxication as well as recognition of concomitant medications or medical conditions that may directly alter the pharmacokinetic profile of digoxin, or indirectly alter its cardiac effects by pharmacodynamic interactions remain essential for safe and effective use of digoxin in patients with AF.

Anti-Arrhythmia Agents↗
PubMed2003

Effects of grapefruit juice on intestinal P-glycoprotein: evaluation using digoxin in humans.

STUDY OBJECTIVES: To determine the effects of grapefruit juice on the pharmacokinetics of oral digoxin, a P-glycoprotein substrate not metabolized by cytochrome P450 3A4, in healthy volunteers, and to assess whether polymorphic multidrug-resistance-1 (MDR1) expression contributes to interindividual variability in digoxin disposition. DESIGN: Prospective, open-label, unblinded, crossover study. SETTING: University research center. SUBJECTS: Seven healthy adult volunteers (four men, three women). INTERVENTION: Each subject received a single oral dose of digoxin 1.0 mg with water or grapefruit juice with at least a 2-week washout between treatments. During the grapefruit juice phase, juice was administered 3 times/day for 5 days before digoxin administration to maximize any effect on P-glycoprotein. MEASUREMENTS AND MAIN RESULTS: Digoxin pharmacokinetics in the presence and absence of grapefruit juice were compared. The MDR1 exon 26 C3435T genotype was determined by real-time polymerase chain reaction. Compared with water, grapefruit juice significantly reduced the digoxin absorption rate constant (3.0 +/- 2.4 to 1.2 +/- 1.0 hr(-1), p<0.05) and increased absorption lag time (0.32 +/- 0.12 to 0.53 +/- 0.34 hr, p<0.05). Grapefruit juice did not affect digoxin maximum concentration (Cmax), area under the curve (AUC), elimination half-life, or renal clearance. The effect of grapefruit juice on digoxin Cmax (-45% to +41%) and AUC(0-4) (-29% to +25%) varied substantially among subjects and was inversely correlated with the values during the water phase. Trends toward higher digoxin Cmax AUC, and absorption rate constant during the water phase were found in CC homozygotes compared with subjects carrying a T allele. CONCLUSION: Inhibition of intestinal P-glycoprotein does not appear to play an important role in drug interactions involving grapefruit juice. Interindividual variability in response to grapefruit juice may be related to the balance of intestinal drug uptake and efflux transport.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMedDate not supplied

Age-related differences in digoxin toxicity and its treatment.

Digoxin toxicity remains a common medical problem for both adults and children. In addition to a vastly improved understanding of the mechanisms for digoxin action on the heart, there are now data which clearly demonstrate that there are potentially important developmental differences in both the pharmacodynamics and pharmacokinetics of digoxin which have a direct impact on its efficacy and toxicity profile. The developmental pharmacokinetics of the drug have been extensively studied such that profiles for age-dependent differences in the apparent volume of distribution, plasma and renal clearance and elimination half-life now exist. It is these data which have also produced the current age-specific dosing guidelines for the therapeutic administration of digoxin in various paediatric subpopulations. Despite this new knowledge, both accidental and iatrogenic digoxin toxicity still occurs in paediatric patients, with potentially life-threatening arrhythmias being produced when steady-state serum digoxin concentrations exceed 5.1 nmol/L. Consequently, the clinician may be faced with the decision to use antidotal therapy with digoxin-specific Fab fragments (d-Fab). This article reviews the developmental basis for digoxin disposition and its pharmacological and toxic effects. Additionally, the treatment of acute digoxin toxicity in children is reviewed, especially as pertains to the therapeutic use of d-Fab.

Adolescent↗
PubMed1988

Pharmacokinetic interactions with digoxin.

Numerous pharmacological agents have been shown to produce clinically significant pharmacokinetic interactions with digoxin. Drugs which reduce digoxin absorption include the antacids aluminium hydroxide, magnesium hydroxide and magnesium trisilicate, the antidiarrhoeals kaolin and pectin, the hypocholesterolaemic agent cholestyramine and the chemotoxins cyclophosphamide, vincristine and bleomycin. Certain antibiotics including sulphasalazine, neomycin and aminosalicylic acid reduce digoxin absorption while others, including erythromycin and tetracycline, increase the bioavailability of digoxin in some patients. Capsule preparations of digoxin in solution are less subject to several of the interactions which affect the absorption and bioavailability of digoxin tablets. Various drugs induce alterations in the volume of distribution and clearance of digoxin. Cardiac patients receiving digoxin therapy are particularly prone to interactions with commonly co-administered medications such as the antiarrhythmics quinidine and amiodarone, the calcium channel blockers verapamil and nifedipine, and possibly some vasodilating agents. Studies of digoxin interactions have yielded discrepant results, indicating the need for careful analysis of investigational design before arriving at clinical conclusions.

Digoxin↗
PubMed1982

Quinidine and digoxin. An important interaction.

An increase in serum digoxin concentration occurs in 90% of patients given quinidine. On average, the serum digoxin doubles during treatment with therapeutic doses of quinidine. Almost every patient treated with quinidine will have a decrease in the renal clearance of digoxin and many will have a decrease in the volume of distribution of digoxin. Whether changes in the inotropic effect of digoxin occur during concurrent quinidine administration is an unsettled area. However, gastrointestinal and cardiac toxicity, which closely resemble digitalis toxicity, often occur when quinidine causes the serum digoxin concentration to rise. These effects subside when the digoxin dose is reduced. Therefore it is prudent to monitor serum digoxin concentrations during concomitant quinidine treatment and to adjust the digoxin dose according to the results. When the toxicity is severe or dose adjustment is difficult, another antiarrhythmic drug should be selected.

Digoxin↗
PubMed1987

Pharmacokinetics of felodipine and effect on digoxin plasma levels in patients with heart failure.

Some calcium antagonist drugs used in hypertension and cardiac diseases have been shown to increase plasma digoxin levels mainly as a result of reduced renal clearance. Felodipine is a new dihydropyridine calcium antagonist drug with cardiovascular effects, whose pharmacokinetics and effects on plasma digoxin levels have been studied in patients with left ventricular failure. 12 patients (11 men) on long term digoxin therapy were given 2.5 or 5 mg felodipine bid for 7 days followed by 1 week on 10mg bid. Plasma levels of digoxin and felodipine were measured before dosage and 30, 60 and 90 minutes and 2, 3, 4, 6, 8, 10 and 24 hours after the first dose and after 1 week of therapy (steady state). The area under plasma concentration versus time curve was calculated after the first dose and in steady state both for digoxin and felodipine. The absorption characteristics Cmax and Tmax were calculated both for felodipine and digoxin on the different felodipine doses. There was a linear relationship between dose and plasma level of felodipine. Plasma half-life in the 4- to 10-hour period of felodipine was 5.5 hours after a 10mg single dose, and 12 hours after 10mg bid. Felodipine 2.5mg, 5mg and 10mg all transiently increased peak plasma digoxin concentrations (by about 40%) at 1 hour after intake. Urinary excretion of digoxin during the day was unchanged, but impaired renal clearance may account for the transient increase in digoxin plasma level after felodipine.

Aged↗
PubMed1981

Digoxin transport in the distal nephron of rats during saline diuresis.

The nephron segments involved in the renal tubular transport of digoxin and the direction of transport in each segment were evaluated using renal micropuncture techniques in 11 rats made diuretic by i.v. infusion of .85% saline. Tubular fluid was collected from 4 different sites along the nephron: late proximal, early distal, late distal, and ureter. The concentrations of 3H-digoxin and 14C-inulin were measured in each sample and the reabsorption of water and efflux of digoxin were calculated. Water was removed from the lumen along the entire length of the nephron and only 2.53 +/- 0.3% of the filtrate was excreted in the urine. Digoxin was also absorbed in the proximal convoluted tubule and in the loop of Henle. About 1/3 of the filtered drug exited in these early nephron segments probably by passive diffusion. In the distal convoluted tubule, digoxin was added to the tubular fluid. The fraction of digoxin present in the lumen increased form 64 +/- 3.8% of the filtered load at early distal site to 78.7% +/- 4.8% at late distal site indicating that an amount equal to 15% of filtered digoxin entered the tubule. This influx occurred against a concentration of 3-5, suggesting the existence of a carrier mediated or active transport mechanism in this nephron segment. Transport of digoxin beyond the late distal puncture site was negligible. The collecting duct appeared to be relatively impermeable to the drug since a concentration gradient of 30 or greater failed to cause its diffusion out of the tubule. The data indicate bidirectional transport of digoxin in the rat nephron. Efflux occurs primarily in the early nephron segments while net influx is limited to the distal convoluted tubule.

Animals↗
PubMed1988

Mechanisms of digoxin-amiodarone interaction in the rat.

Amiodarone and digoxin are often used in combination and clinical experience suggests that amiodarone may increase serum digoxin levels and toxicity. We have investigated the influence of amiodarone on digoxin pharmacokinetics and tissue distribution in the rat. Forty-nine rats were injected with 10 mg/kg amiodarone sc three times a day for 7 days, while 49 others were injected with saline only. On the eighth day, all the rats received 0.5 mg/kg digoxin ip; 4, 5, 6, 7, 8, 10, and 12 hr later, groups of 7 amiodarone-pretreated and control animals were sacrificed, and plasma, heart, liver, muscle, brain, and kidney digoxin concentrations measured by radioimmunoassay. Data were analyzed by two-way ANOVA, with group comparisons using the Waller-Duncan multiple comparison procedure. Digoxin levels were significantly higher in the plasma, heart, muscle, and kidney of the amiodarone-pretreated rats at most points of measurement (P less than 0.05) whereas liver digoxin levels were elevated at 8, 10, and 12 hr. Kidney/plasma, heart/plasma, muscle/plasma, and especially liver/plasma ratios in the control groups significantly exceeded the values found in the amiodarone-pretreated group at most time points. Concentrations of digoxin in brain were not changed. This suggests that the volume of distribution is significantly altered in the amiodarone-pretreated group. Amiodarone increases plasma digoxin levels in rats as it does in humans, but the mechanism is unclear.

Algorithms↗
PubMed2004

[Inappropriate blood levels of digoxin in a study of 2,849 patients from a teaching hospital: the influence of age and sex].

OBJECTIVES: Digoxin is used to treat congestive heart failure and atrial fibrillation. Blood levels need to be monitored to optimize therapeutic performance, detect noncompliance and reduce toxicity. The aim of this study was to evaluate the use of digoxin by measuring blood levels of this drug. The influence of sex and age were also considered. PATIENTS AND METHOD: A retrospective study reviewed determinations of blood digoxin concentration in hospitalized and ambulatory patients with congestive heart failure, atrial fibrillation, or both, seen at the University of Granada Teaching Hospital (Spain) from 1992 to 2002. A chi square test was applied to results. RESULTS: A total of 5,623 laboratory tests for digoxin were done for 2,849 adult patients. Patients whose medical record was incomplete were excluded, and the final sample consisted of 2,629 patients. The 55.4% had inappropriate blood levels of digoxin. Inappropriate concentrations to digoxin were significantly higher in women (p < 0.001). The percentage of patients with high levels of the drug was significantly greater among men (p < 0.001). Very low concentrations (< 0.5 ng/ml) were found in 16% of the patients, with no significant difference between sexes. CONCLUSIONS: We detect a large percentage of older patients with inappropriate levels of digoxin in blood. Women were more likely than men to have high levels to digoxin in blood. There is evidence that therapeutic monitoring of blood levels of digoxin is not done as often as is advisable; this has implications for the care of patients being treated with this drug.

Adult↗
PubMed1999

[The influence of digoxin treatment on the statistical distribution of R-R intervals in atrial fibrillation].

Functional refraction of atrio-ventricular node and the phenomenon of concealed conduction are basic factors which determine the frequency of ventricular beats as well as the duration of R-R intervals in atrial fibrillation. R-R intervals may be ordered according to their size and presented graphically in the form of histograms. The morphology of histograms depends on the ability of A-V node. Digoxin influences the morphology of histograms of R-R intervals, which may have a diagnostic value and become a therapeutic indicator. The purpose of the study was to evaluate the correlation between the morphology of histograms and digoxin serum concentration, as well as the clinical treatment with digoxin. In the study a classification was used which divided R-R intervals into 4 types and several sub-types. The study covers 91 patients treated with digoxin upon whom 161 histograms were made. Two groups of patients were studied: A-patients in whom digoxin concentration was determined, B-patients in whom treatment with digoxin was evaluated on the basis of their clinical condition. The study confirmed a hypothesis that treatment with digoxin causes specific changes in the statistical distribution of R-R intervals even though no strict correlation was found between the direction of these changes and the digoxin serum concentration. The dependence, however, was observed between histograms of R-R intervals in atrial fibrillation and the clinical course of treatment with digoxin.

Adult↗
PubMed1975

Tritiated digoxin metabolism after prior treatment with propranolol or diphenylhydantoin sodium.

Digitalis-induced arrhythmias can be suppressed by intravenous potassium, diphenylhydantoin sodium and propranolol. As it is known that hyperkalemia can interfere with the myocardial uptake of digoxin, this study was performed to determine whether diphenylhydantoin sodium or propranolol could exert any antiarrhythmic effect by altering the metabolism of 3H-digoxin and, in particular, the accumulation of the glycoside by cardiac muscle. Three groups of anesthetized dogs were given 6 muCi 3H-digoxin per kilogram intravenously, and in two groups 15 mg/kg diphenylhydantoin sodium or 3 mg/kg propranolol were injected intravenously 15 minutes prior to the glycoside. The concentration of labelled digoxin was measured in plasma up to one hour, and then tissues were removed and analyzed for digoxin content. Diphenylhydantoin sodium did not influence myocardial uptake of digoxin. It is considered its suppressant action on digitalis-induced arrhythmias is not due to any effect on the cardiac accumulation of digoxin. Propranolol did reduce the myocardial uptake of digoxin, but this was not considered of sufficient magnitude to be the main factor in suppressing arrhythmias induced by digitalis. These studies provide evidence that both diphenylhydantoin sodium and propranolol do not have a suppressant effect on digitalis-induced arrhythmias by virtue of any significant interference with the uptake of digoxin by myocardial tissue.

Animals↗
PubMed1998

[Determination of digoxin-like immunoreactive substances in sera of 15 elder patients with cardiac insufficiency].

The presence of a higher concentration of digoxin-like immunoreactive substances (DLIS) in human serum have been reported in a number of pathophysiological conditions. DLIS can react with anti-digoxin antibodies when determination of serum digoxin was performed with immunoassay. It may falsely elevate the serum digoxin concentration and is troublesome in the therapeutic monitoring of digoxin. The apparent digoxin concentrations (DLIS) in serum were determined in 15 elder patients with cardiac insufficiency by fluorescence polarization immunoassay (FPIA). The lowest measurable concentration, defined as the concentration that could be distinguished from zero with 95% confidence, was 0.256 nmol.L-1. Steroids and drugs commonly administered with digoxin showed no significant cross-reactivity. In these patients, the positive ratio for determination of DLIS was 46.7% (7 in 15 cases), and its mean serum concentration was 0.55 +/- 0.44 nmol.L-1 (range 0.26-1.52 nmol.L-1). The results were well consistent with that obtained by Dasgupta et al. In conclusion, there are certain increased concentrations of DLIS in the sera of elder patients with cardiac insufficiency, suggesting that digoxin levels measured by immunoassay method must be interpreted carefully in these patients after treatment with digoxin or other digitalis preparations.

Aged↗
PubMedDate not supplied

[Antidigoxin Fab fragments and digoxin monitoring: a challenge for the biologist].

Following administration of anti-digoxin Fab fragments, monitoring unbound digoxin concentrations may help ensure appropriate dosing, and prevent recrudescent toxicity. Ultrafiltration by using Centrifree system and measurement of digoxin in the ultrafiltrate is considered as reference technique. However, ultrafiltration method is cumbersome, costly, and some immunoassays are affected by matrix differences. Another approach is to analyse the serum directly by digoxin immunoassays without ultrafiltering it. The validity of results obtained depends on the architecture of the immunoassay and the amount of Fab in the sample. The old radioimmunoassays and usually the other competitive immunoassays give inaccurate results. The fluorescence polarization immunoassay (FPIA) slightly underestimates the total digoxin concentrations. Total digoxin levels obtained at 24 hours and 48 hours after treatment permit measurement of the half-life of digoxin Fab complexes and can be used to estimate when the patient can be redigitalized, if necessary. The sequential immunoassays usually overestimate the free digoxin concentrations. The differences observed are >25% and cannot be explained solely by albumin binding (normal range, 20% +/- 5%). To date, ultrafiltration remains the best strategy for accurate determination of digoxin concentrations in the presence of antidigoxin Fab fragments.

Aged↗
PubMedDate not supplied

Intestinal absorption of digoxin and interaction with nimodipine in rats.

It is known that digoxin, which is a liposoluble cardiac glycoside, is well absorbed from intestine. In the present study, the absorption rates of digoxin from rat duodenum and the proximal and terminal parts of small intestine were determined in vitro. The isolated everted duodenum and intestinal sacs were put into oxygenated Tyrode solution at 37 degrees C. The Tyrode solution on the outer, mucosal side of intestinal segments contained 0.3 microM digoxin. Samples from the internal serosal side of the intestinal sacs were taken at 30, 60 and 120 min after the start of the experiments. The concentration of digoxin in the samples of fluid were determined using a radioimmunoassay method. The effect of nimodipine (0.1 and 0.2 mM) on digoxin absorption was also evaluated on the terminal segment of rat intestine. The interaction of nimodipine (0.5 mg/kg) and digoxin (0.2 mg/kg) was investigated in vivo when they were given perorally to rats. The duodenal absorption of digoxin was lower than in the small intestine. The highest absorption occurred in the terminal segment of the small intestine. Nimodipine increased the absorption of digoxin from the terminal segment of intestine in vitro, while it did not affect the serum digoxin concentration in vivo.

Administration, Oral↗
PubMed2004

Cross-sectional study of heart failure therapy with angiotensin converting enzyme inhibitors and digoxin.

OBJECTIVE: The aim of the present study is to show a better short-term (2 weeks) clinical improvement in patients with heart failure (HF) who are receiving angiotensin converting enzyme inhibitors (ACEIs) (with or without digoxin) when compared to the standard therapy excluding ACEIs. METHODS: The study was conducted in Al-Gamhuria Teaching Hospital, Aden, Yemen, from January to July 2003. In this study, 78 patients with HF were enrolled into 3 therapeutic groups (ACEIs alone, ACEI and digoxin and digoxin alone) and their responses within 2 weeks were recorded. Exclusion criteria were as follows: thyroid disorders, gastrointestinal disturbances (diarrhea, malabsorption), electrolyte unbalanced (unless corrected) and insufficient data. Serum creatinine was measured at the beginning and after 10 days. In addition, the patients' body weight and age were recorded. Criteria for a complete improvement within 2 weeks were the occurrence of the following: 1) The relief of pulmonary congestion, 2) Decrement in heart rate to less than 74 +/- 5, 3) Disappearance of the lower limb edema, and 5) Recorded positive electroencephalogram change. Partial amelioration was recognized if only 2 or 3 of the preceding criteria were observed. RESULTS: Nine patients received digoxin alone, while 40 patients were treated with ACEIs and digoxin. Treatment with ACEIs without digoxin was observed in 29 patients. The discrepancy between the number of patients was necessitated by the need of patients with HF. This last category of treatment regimen produced better clinical improvement (complete with 10.1%, partial with 24.3%) compared to the digoxin group without ACEI (complete 2.5% or partial 5.1%). Nevertheless, the addition of digoxin to an ACEI increased this ratio (17.8% for complete and 28.2% for partial improvement). A 49.3% increase in serum creatinine was observed after 10 days in 25 HF patients, who were randomly selected and followed up (the baseline concentration was 99.75 +/- 9.9 umol/L, while the level after 10 days was 148.97 +/- 19.8 umol/L, p=0.005). CONCLUSION: We confirmed that short-term use of ACEI regimens has a superior effect on the therapy of HF (34.4% complete and partial response) as compared to the therapy of not using ACEI (7.6% had a complete and partial response). The combination of ACEI and digoxin has resulted in the best outcome (46% had a complete and partial response). However, we also noticed a significant rise in serum creatinine by 49% concomitant with the use of ACEI (the baseline concentration was 99.75 +/- 9.9 um/L, while the level after 10 days was 148.97 +/- 19.8 umol/L, p=0.005).

Administration, Oral↗
PubMed1991

Some pharmacokinetic and pharmacodynamic interactions between digoxin and gentamicin.

Some pharmacokinetic and pharmacodynamic interactions between digoxin and gentamicin were studied in experiments on rabbits, guinea-pigs and cats. An increase of digoxin serum levels and changes in some basic pharmacokinetic parameters of digoxin (t1/2 alpha, t1/2 beta, AUC, AL) were established in gentamicin-pretreated rabbits, the changes being dependent on the dose and schedule of administration. Most pronounced were the changes in digoxin kinetics during simultaneous 5-day treatment with digoxin (0.035 mg/kg i. p.) and nontoxic doses (10 and 2 mg/kg) of gentamicin. The toxicity of digoxin in guinea-pigs, assessed by lethal doses of digoxin, was increased only after the highest dose of gentamicin (100 mg/kg), while after nontoxic or close to therapeutic doses (10 and 2 mg/kg) of gentamicin the digoxin toxicity was not changed or was even decreased. Digoxin decreased the nerve-muscle blocking effect of gentamicin on cat ischiadicus-gastrocnemius preparation. The possible mechanisms involved are discussed.

Animals↗