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PubMed1976

Myocardial digoxin uptake: dissociation between digitalis-induced inotropism and myocardial loss of potassium.

The time course of myocardial uptake of digoxin, of increase in inotropic effect and of changes in myocardial potassium content were studied following a single intravenous dose of digoxin. Nineteen dogs with intact circulation were investigated by the use of a biopsy technique which allowed samplings before and 10, 30, 60, and 90 min after administration of digoxin. The myocardial concentration of digoxin was 196 X 10(-9) mol/kg 10 min after administration of digoxin. Uptake continued at a slower rate, maximum concentration being 293 X 10(-9) mol/kg at 60 minutes. The inotropic effect increased parallel with the uptake of digoxin; 10 min after digoxin, contractility was 127% of the control value and this increased to 139% at 90 minutes. Myocardial potassium content was slightly increased 10 min after digoxin, suggesting an initial stimulation of membrane Na+-K+ ATPase. A subsequent significant fall in the myocardial potassium content probably reflects ATPase inhibition. The temporal dissociation between the early onset of the positive inotropic effect and the delayed inhibition of membrane Na+-K+ ATPase indicates that inotropism of digitalis glycosides is not mediated by the same binding site as that responsible for inhibition of Na+-K+ ATPase.

Animals↗
PubMed1977

The effect of phenytoin on the tissue concentrations of digoxin in the rat.

Rats treated chronically with digoxin were treated with two different dose levels of phenytoin, either as a single dose or chronically. Digoxin concentrations were measured by radioimmunoassay in the serum, urine, heart, muscle, liver, and the kidney. Chronic treatment with the high dose of phenytoin significantly increased the digoxin levels in the serum and tissues and decreased the renal clearance of digoxin. The low dose of phenytoin significantly reduced the serum and tissue levels of digoxin and increased the renal clearance. Single doses of phenytoin had a tendency to cause similar changes. Levels of digoxin were altered during the phenytoin treatment. In contrast to man, digoxin is extensively metabolized in the rat. Enzyme induction in connection with low phenytoin dosage and inhibition by high dosage is the suggested mechanism. It can be speculated that the tissue distribution and excretion of digoxin are altered.

Animals↗
PubMed2006

P-glycoprotein and an unstirred water layer barring digoxin absorption in the vascularly perfused rat small intestine preparation: induction studies with pregnenolone-16alpha-carbonitrile.

Digoxin, a substrate of P-glycoprotein (Pgp) and cytochrome P450 3a (Cyp3a), was used to illustrate the inductive effects of pregnenolone-16alpha-carbonitrile (PCN), a ligand of the pregnane X receptor, on the absorption and disposition of [3H]digoxin in the vascularly perfused rat small intestine preparation. Although increased Cyp3a protein was observed with Western blotting analysis after PCN treatment, metabolism of digoxin to the digoxigenin bis-digitoxoside metabolite in the rat small intestine remained insignificant (<4% dose). PCN pretreatment significantly decreased blood perfusate [3H]digoxin concentrations for both systemic and intraluminal administrations of [3H]digoxin due to increased Pgp levels. The apical secretion by Pgp increased at 90 min with PCN treatment, from 11.2 +/- 5.1% of dose to 20.1 +/- 8.6% of dose after systemic administration of [3H]digoxin; this increase was, however, statistically insignificant (P = 0.13) because of the high variability among preparations. When the composite data for the control and PCN-treated preparations were fit to published physiologically based pharmacokinetic models: the traditional model and the segregated flow model, suboptimal parameters were obtained. The data were further fit to expanded models with a bilayer membrane compartment housing the Pgp adjacent to the apical membrane, or an unstirred water layer (UWL) external to the apical membrane. The models with the UWL yielded improved fits and reasonable parameters associated with digoxin absorption, suggesting that the UWL posed as a barrier for digoxin absorption. Similar results were obtained with the segmental models (the segmental traditional model and the segmental segregated flow model) using the UWL, when heterogeneous distributions of Pgp in the duodenum, jejunum, and ileum were considered.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2004

Characterization of the neutralizing activity of digoxin-specific Fab toward ouabain-like steroids.

Digoxin-specific Fab (Digibind) is a mixture of antidigoxin Fab fragments prepared from sheep sera and is used as a treatment for digoxin poisoning. Digoxin-specific Fab has been shown to neutralize an endogenous Na+/K+ ATPase inhibitor (endogenous digoxin-like Na+/K+ ATPase regulatory factor; EDLF) in rats and humans and to lower blood pressure. Although the exact structure of EDLF is unknown, compounds identical to or structurally related to ouabain, bufalin, and marinobufagenin have been detected in mammalian plasma. In this study, some structural characteristics of EDLF were inferred from the ability of digoxin-specific Fab to neutralize the Na+/K+ ATPase inhibitory activity of several known cardenolides and bufodienolides. Additional structural information was obtained from [3H]ouabain binding and enzyme-linked immunosorbent assay experiments. Digoxin-specific Fab had the ability to interact to some extent with all of the cardenolides and bufodienolides tested. However, digoxin-specific Fab was more than 20-fold more potent in neutralizing ouabain and bufalin than marinobufagenin. The antihypertensive effect of digoxin-specific Fab seen in preeclampsia and animal models of hypertension may therefore be due to a molecule identical to or structurally similar to ouabain or bufalin.

Animals↗
PubMed2003

Effects of digoxin on left atrial function in heart failure.

OBJECTIVE: To investigate the effects of digoxin on left atrial (LA) function in patients with congestive heart failure and dilated left atria. PATIENTS: 30 patients with enlarged left atrium (maximum LA diameter > 4 mm) caused by heart failure (New York Heart Association functional class III or IV) were studied before and after treatment with digoxin (0.25 mg orally for 12 days). Digoxin was also administered to 30 normal participants who served as controls. MAIN OUTCOME MEASURES: LA active (AEF) and passive emptying fractions (PEF), reservoir fraction (RF), kinetic energy (KE), and mean velocity of circumferential atrial fibre shortening (Vcf) were calculated from echocardiographic measurements of LA volumes and transmitral Doppler flow velocities at baseline and on the third, sixth, eighth, and 12th day after digoxin administration. RESULTS: LA AEF, PEF, RF, KE, and Vcf were significantly lower in patients than in controls (p < 0.001). LA AEF, PEF, RF, KE, and Vcf increased significantly both in patients and controls after digoxin administration (p < 0.001). This increase was greater in patients than in controls (p < 0.001). KE was linearly correlated with LA volume at the onset of atrial systole in all participants. The slope and the intercept of this relation were significantly increased after digoxin both in patients and in controls (p < 0.001). CONCLUSIONS: LA performance is impaired in patients with heart failure. Dilated atria manifest atrial failure. Digoxin improves LA performance and LA contractility both in dilated and in normal atria. The effects of digoxin on LA contractility are augmented in the failing atria compared with the normal atria.

Adult↗
PubMed1983

Digoxin-amiodarone interaction: in vivo and in vitro studies in rats.

Amiodarone is a new antiarrhythmic drug, commonly coadministered with digoxin in various cardiac disorders. Amiodarone caused a 10-fold increase of serum digoxin in rats, when the two drugs were simultaneously administered. Amiodarone significantly reduced digoxin uptake by renal cortical slices in the rat, and failed to reduce digoxin uptake by either heart or diaphragmatic muscle. The inhibition of the renal tubular uptake of digoxin caused by amiodarone may explain in part the increased serum digoxin concentration observed in vivo. Close resemblance was found between the mechanisms involved in the amiodarone-digoxin interaction, and those of digoxin interaction with either quinidine or verapamil.

Amiodarone↗
PubMed1989

The effect of inhibitors of endogenous opioid degradation, bacitracin, bestatin, captopril, and D-phenylalanine, on digoxin-induced arrhythmias in guinea pigs.

The purpose of this study was to investigate the effect of inhibition of endogenous opioid degradation on digitalis-induced arrhythmias, utilizing the inhibitors bacitracin, bestatin, captopril, and D-phenylalanine. Guinea pigs, anesthetized with pentobarbital, 50 mg/kg i.p., and breathing spontaneously received intracerebroventricular (i.c.v.) injection of bacitracin (6.8 mg/kg), bestatin (1 mg/kg), captopril (2 mg/kg), D-phenylalanine (1.2 mg/kg) or the diluent, saline. Digitalis arrhythmias were induced by a 50 micrograms/kg i.v. bolus of digoxin followed by 500 micrograms.kg-1.h-1 i.v. Bacitracin and bestatin, but not captopril or D-phenylalanine, significantly (p less than 0.05) altered the relationship between the digoxin dose and the first occurrence of arrhythmias, i.e., digoxin-induced ventricular arrhythmias became manifest at lower digoxin doses. The mean digoxin dose and ED50s, at which arrhythmias first occurred, were significantly (p less than 0.05) reduced by bacitracin and bestatin. The findings were similar for fatal arrhythmias, although D-phenylalanine appeared to decrease the digoxin dose at the development of fatal arrhythmias. The opioid antagonist naloxone, in a 50 micrograms/kg bolus and 50 micrograms.kg-1.h-1 i.c.v., completely prevented these effects of bacitracin and reduced the effect of bestatin. The relationship to arrhythmias could not be ascribed to an effect on blood pressure, as the blood pressure response to digoxin was the same in bestatin, D-phenylalanine, and control groups. To examine whether systemic administration of an inhibitor of opioid degradation had similar effects, a second protocol was selected with systemic administration of bacitracin because it altered the dose effect relationship after i.c.v. administration and systemic concentrations could be readily attained. Bacitracin, in a 13.5 mg/kg i.v. bolus and 135 mg.kg-1.h-1 i.v., was followed by 100 micrograms/kg digoxin i.v. every 15 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopeptidases↗
PubMed1992

Oxygen transport during anemic hypoxia in pigs: effects of digoxin on metabolism.

We tested whether digoxin would limit tissue hypoxia during severe anemia by improving peripheral O2 distribution or decreasing O2 demands. Hematocrit (Hct) was reduced in eight control and eight digoxin-treated pigs from 27-28% to 17-18, 11-12, and 7-8%. Whole body and hindlimb blood flow, O2 transport, O2 extraction, and O2 consumption and serum catecholamines (epinephrine and norepinephrine) were determined at each Hct. Arterial and femoral venous lactate and O2 deficit were obtained to reflect tissue hypoxia. Cardiac output was significantly greater (P less than 0.05) with digoxin, as expected, but there were no differences in hindlimb blood flow. Also, whole body and hindlimb O2 extractions were equal in both groups for similar levels of O2 transport, suggesting that digoxin did not alter the relationship of O2 flow to metabolism in regional circulations. As whole body O2 consumption fell, controls accumulated more (P less than 0.05) O2 deficit and arterial lactate than the digoxin group. Furthermore, the slope demonstrating the linear increase of lactate with respect to O2 deficit was much steeper in controls (y = 1.11 + 0.06x) than in digoxin (y = 1.36 + 0.02x), suggesting that there were differences in the degree of tissue hypoxia for comparable O2 deficit. This may be attributed to the marked differences in catecholamine response: epinephrine was higher in controls at Hct of 7-8% and norepinephrine was higher at Hcts of 11-12 and 7-8%. Digoxin may have inhibited the release of catecholamine or reduced the stimulus for catecholamine secretion during anemia. We speculate that digoxin markedly improved the balance between peripheral O2 supply and demand during anemia by inhibiting catecholamine thermogenesis, thereby decreasing O2 demands. This may explain some of the salutary effects of glycosides in high-output cardiac failure with normal ventricular function.

Anemia↗
PubMed1998

Effects of ketoconazole on digoxin absorption and disposition in rat.

Digoxin, a cardiac glycoside, is a substrate of the multidrug transporter P-glycoprotein (Pgp), and in rats has also been identified as a substrate for cytochrome P450 3A (CYP3A). Ketoconazole, an antifungal agent, was shown to inhibit Pgp in a multidrug-resistant cell line, and is known to be a potent inhibitor of CYP3A. Here, we determined the effects of ketoconazole on digoxin absorption and disposition in rats. Digoxin was administered intravenously or orally with or without a concomitant oral dose of ketoconazole. When given intravenously, digoxin AUC increased from 93 +/- 22 to 486 +/- 26 microg x h/l with ketoconazole administration. Similarly, ketoconazole raised the AUC of orally administered digoxin from 63 +/- 17 to 411 +/- 50 microg x h/l. Concomitant ketoconazole administration prolonged digoxin elimination, yielding a nonlinear pharmacokinetic profile. Using time-averaged values, digoxin bioavailability increased from 0.68 +/- 0.18 to 0.84 +/- 0.10, while mean absorption time was reduced from 1.1 +/- 0.4 to 0.3 +/- 0.1 h. Thus, in rats, ketoconazole increases digoxin plasma concentrations, rate of absorption and bioavailability. Although the effects of ketoconazole on AUC could be explained by inhibition of both CYP3A and Pgp, which cannot be differentiated in this study, the decreased mean absorption time can only be explained by inhibition of Pgp in the intestine.

Animals↗
PubMed2004

Safety of transvenous temporary cardiac pacing in patients with accidental digoxin overdose and symptomatic bradycardia.

BACKGROUND: Patients with digoxin intoxication may need transvenous temporary cardiac pacing (TCP) when symptomatic bradyarrhythmias are present. However, it has been reported that TCP might be associated with fatal arrhythmias in patients with acute digitalis intoxication caused by attempted suicide. The aim of this study was to assess the safety of TCP in patients with accidental digoxin-related symptomatic bradyarrhythmias. MATERIALS AND METHODS: Seventy patients (30 men; age 74 +/- 12 years) were enrolled in this retrospective study. Patients were divided into two groups: group 1 with TCP and group 2 without TCP. A digoxin overdose was defined as a serum digoxin level higher than 2.0 ng/ml combined with the presence of digoxin-related symptoms. Detailed clinical characteristics were reviewed on the basis of the medical records. RESULTS: Group 1 included 24 patients (34.3%, 10 men). The rhythms prior to pacemaker insertion in group 1 included sinus arrest with junctional bradyarrhythmias (n = 9), atrial fibrillation with a slow ventricular rate (n = 11), and high-degree atrioventricular block (n = 4). The mean duration of pacemaker implantation was 5.8 +/- 2.9 days (2-12 days). There was no major arrhythmic event or mortality after TCP in group 1. Two patients in group 2 (4%) died of ventricular tachyarrhythmias. Group 1 had a higher level of blood urea nitrogen (45.1 +/- 26.0 vs. 33.4 +/- 19.3 mg/dl), of left ventricular ejection fraction (68 vs. 56%), and of digoxin (4.4 +/- 2.1 vs. 3.4 +/- 1.3 ng/ml) but a lower serum calcium level (8.7 +/- 0.6 vs. 9.1 +/- 0.8 mg/dl). CONCLUSION: TCP was safe for patients with a digoxin overdose complicated by symptomatic bradycardia and should be recommended in such situations. However, this conclusion does not apply to acute digoxin intoxication as a result of attempted suicide.

Aged↗
PubMed1981

The kinetics of red blood cell electrolyte alterations following digoxin administration. A report of two pediatric cases.

Serial determinations of plasma and red blood cell (RBC) Na+, K+, and Mg++ concentrations were obtained in 2 children following digoxin administration. Treatment with digoxin was associated with a 50-70% increase in the RBC Na+ concentration, whereas the RBC K+ concentration decreased by 7-10%. RBC electrolyte changes paralleled plasma digoxin levels in the child who was digitalized slowly, whereas the maximum shift in RBC electrolyte concentration occurred 48 h after peak plasma digoxin concentrations were observed in the child who had received a single dose of digoxin. These results suggest that Na+/K+-ATPase inhibition may continue after clearance of digoxin from the plasma. The use of plasma digoxin concentration to diagnose toxicity may be limited in the special case of children who have received a single large dose of digoxin.

Child, Preschool↗
PubMed1987

Effects of digoxin on diaphragmatic strength generation in patients with chronic obstructive pulmonary disease during acute respiratory failure.

We studied the effects of digoxin, a compound that has an inotropic effect on the myocardium, on diaphragmatic function in 8 patients with chronic obstructive pulmonary disease. All the patients were in acute respiratory failure and were artificially ventilated. Diaphragmatic strength was assessed by measuring the transdiaphragmatic pressure generated at functional residual capacity during bilateral supramaximal electrical stimulation of the phrenic nerves. The latter were stimulated before and at 45 and 90 min after administration of digoxin (0.02 mg/kg infused for 10 min). In all the patients, cardiac output was measured by the thermodilution technique using a Swan-Ganz catheter placed in the pulmonary artery. Arterial blood gases and pH were maintained within normal range by mechanical ventilation. In all the patients, digoxin plasma levels reached the therapeutic range (mean values, 2.82 +/- 0.17 and 2.90 +/- 0.20 nmol/L at 45 and 90 min, respectively) after digoxin administration. Diaphragmatic strength improves significantly after digoxin administration, the transdiaphragmatic pressure for an identical phrenic stimulation increasing by 19.5% (p less than 0.001) on the average. This increase was noted 45 and 90 min after digoxin administration. We conclude that digoxin has a potent effect on diaphragmatic strength generation that may be beneficial in patients with chronic obstructive pulmonary disease during acute respiratory failure. Furthermore, this inotropic positive effect of digoxin on the diaphragm, as previously observed for the myocardium, emphasizes the similarities between these 2 contractile tissues.

Action Potentials↗
PubMed1974

The central nervous system as a site of action for the coronary vasoconstrictor effect of digoxin.

Digitalis is known to have a vasoconstrictor effect in the coronary circulation. Recent studies have demonstrated that the coronary vasoconstrictor effects of acetylstrophanthidin and digoxin are neurally mediated via alpha adrenergic fibers. In the present study, experiments were done in 20 dogs anesthetized with chloralose and urethane to study the central nervous system as a possible site of action for this vasoconstrictor effect of digoxin. After the intravenous administration of 1.0 mg digoxin, cerebrospinal fluid concentrations of digoxin rose to a peak of 2.3+/-0.4 (SEM) ng/ml at 15 min, temporally corresponding to the peak in coronary vascular resistance change of +20.0+/-2.5% of control in the paced canine heart. Submicrogram digoxin injections into the lateral cerebral ventricle produced a significant increase in coronary vascular resistance, the latter injection producing a peak increase in coronary vascular resistance of 12.4+/-1.2% of control. Cross-perfusion experiments, where the isolated head of the operative dog was perfused from a donor dog receiving digoxin, thus keeping digoxin levels in the remainder of the operative dog very low, showed a similar degree of coronary vasoconstriction. Thus, the central nervous system appears to be an important site of action for the early coronary vasoconstrictor effect of digoxin.

Animals↗
PubMed2001

Lack of citalopram effect on oral digoxin pharmacokinetics.

The effect of chronic administration of citalopram on the single oral dose pharmacokinetics of digoxin was evaluated in 11 healthy adult subjects in an open, one-way crossover study. Subjects received 1 mg digoxin on day 1. Serial blood samples and total urine were collected over 192 hours, followed by an 11-day washout period. On days 22 through 50, subjects received 40 mg citalopram once daily. On day 43, a single dose of 1 mg digoxin was coadministered; again, serial blood samples and total urine were collected over 192 hours after the digoxin dose. There were no statistically significant differences in any of the digoxin pharmacokinetic parameters (AUC(0-->24), AUC(0-->infinity), Cmax, tmax, t(1/2), CL/F, CLrenal, and Ae(0-->infinity)), and the 90% confidence intervals for treatment differences for the parameters (except for tmax) were all within 80% to 125%. Concomitant digoxin administration did not significantly affect citalopram pharmacokinetics. The treatment was well tolerated by all subjects; no serious adverse events and no clinically significant ECG changes were observed. These data suggest that it is unlikely that concomitantly administered citalopram would have any significant effect on serum digoxin concentrations in patients who are receiving chronic digoxin therapy.

Administration, Oral↗
PubMed1981

Maturation of renal tubular transport of digoxin.

Previous data have suggested an age-related increase in renal tubular secretion of digoxin in infants and children receiving long-term digoxin therapy. This phenomenon could be the result of a maturational process or secondary to chronic substrate stimulation. To investigate this question, two groups of 2-week-old paired littermate rats received intraperitoneal injections of either digoxin or an equal volume of normal saline (control) on alternate days until sacrificed at 4, 6, and 8 wk of age. An additional group of 12-wk-old rats were studied as controls. 125I-labeled digoxin uptake was measured in renal cortical slices as the cPM/mg wet tissue slice/medium ratio (S/M). Both digoxin-treated and control rats demonstrated significant age-related increments in digoxin uptake. S/M ratios at 4, 6, 8, and 12 wk in he control group were 1.34 +/- 0.06, 1.39 +/- 0.14, 1.62 +/- 0.18 and 1.93 +/- 0.23, respectively (mean +/- S.D.) (r = 0.81; P less than 0.001). S/M ratios in the digoxin-treated animals at 4, 6, and 8 wk were 1.28 +/- 0.16, 1.33 +/- 0.09, and 1.52 +/- 0.23, respectively (r = 0.50; P less than 0.025), but did not differ significantly at each age from those in the control group. 125I uptake was significantly reduced by both dinitrophenol and sodium azide, as well as by a 100% nitrogen atmosphere. These results indicate that renal tubular transport of digoxin is an age-related energy dependent process which probably is not subject to substrate stimulation.

Age Factors↗
PubMed2001

Factors influencing the prediction of steady state concentrations of digoxin.

The prediction error in the Bayesian analysis program for digoxin was evaluated in Japanese patients, and factors influencing the accuracy were investigated. Serum concentrations of digoxin were monitored two times and were compared with the predicted values obtained by using the Bayesian analysis program. The prediction error at the first time was 43.1%. Although this estimation error was reasonably restored at the second time of monitoring, the prediction error remained at 26.6%. These data suggested that unknown factors not included in the program affected the serum concentration of digoxin. Retrospective research of the digoxin serum concentrations in the patients suggested the coadministration of the drugs, which were the P-glycoprotein modulators, as well as the unexpected alteration of the serum creatinine, were the important factors influencing the prediction of the drug serum concentrations. We next examined the inhibitory effect of quinidine, verapamil and spironolactone on the transcellular transport of digoxin by using human P-glycoprotein overexpressing LLC-GA5-COL150 cells. Quinidine, verapamil and spironolactone could inhibit the transcellular transport of digoxin by 50%. In addition, the reduction of the renal clearance by 50%, which could possibly be caused by this inhibition, led to the increase of 36% in the steady state through concentrations of digoxin in the physiological pharmacokinetic model. In conclusion, the prediction of long-term serum concentration-time profiles of digoxin, based on the Bayesian analysis, will be disturbed by the coadministration of the P-glycoprotein modulators and the unexpected alteration of the serum creatinine.

Adolescent↗
PubMed2005

Pharmacokinetic characterization of transcellular transport and drug interaction of digoxin in Caco-2 cell monolayers.

To characterize the intestinal absorption of digoxin, its transcellular transport and drug interaction activity was investigated using Caco-2 cell monolayers. We examined digoxin transport in the presence and absence of ouabain to determine whether digoxin binding to Na+,K(+)-ATPase affects its transcellular digoxin transport, and evaluated its influx and efflux clearance by model-dependent pharmacokinetic analysis. Transcellular transport in the basal-to-apical direction was greater than that in the opposite direction. In addition, ouabain decreased the cellular accumulation of digoxin, but it did not alter its transcellular transport profile. The observations for transcellular transport and cellular accumulation in the presence of ouabain were used for the pharmacokinetic analysis, which showed that the efflux clearance of digoxin on the apical side of the monolayer was 15 times greater than that on the basal side. Apical-to-basal transport was increased by carvedilol and pimobendan, and these compounds suppressed the efflux clearance on the apical side and the influx clearance on the basal side. These findings indicate that the intestinal absorption of digoxin is primarily dominated by the efflux process on the luminal side of the intestine, and that carvedilol and pimobendan may vary the rate of intestinal digoxin absorption mainly by inhibiting its exsorptive transport.

Biological Transport↗
PubMed1984

An altered distribution and elimination of digoxin in anemic patients and experimentally induced anemic rats.

Digoxin was administered orally to eight anemic patients in their anemic and convalescent stages, and serum digoxin concentration was determined by radioimmunoassay. In the anemic patients a significantly lower level of serum digoxin concentration was observed in anemic state compared with convalescent stage at 72 hours after the drug administration (p less than 0.01). In usual clinical use, a full digoxin effect is expected to be attained as 72 hours. Tritiated digoxin was administered intravenously to anemic and control rats and the tritium in samples of the blood, myocardium and urine were counted in a liquid scintillation counter. The anemic rats showed significantly lower level of serum 3H-digoxin at 6 hours (p less than 0.01) and lower myocardial concentration at 24 hours (p less than 0.01). Larger amount of urinary excretion of 3H-digoxin was observed in the anemic rats 6 hours after the drug administration. No significant difference in fecal excretion of 3H-digoxin was found between the anemic and control rats.

Anemia, Hypochromic↗