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PubMed1989

Effects of digoxin on acetylcholine and norepinephrine concentrations in rat myocardium.

The influence of digoxin on the autonomic nervous system was studied in rats by examining its effects on the levels of acetylcholine (Ach), a parasympathetic marker, and norepinephrine (NE), a sympathetic marker, in the rat myocardium. Ach and NE were measured by high performance liquid chromatography with electrochemical detection (HPLC-ECD). Digoxin was injected subcutaneously every day for 4 weeks. The administration of 0.35, 0.75, and 2.5 mg/kg of digoxin reduced Ach concentrations in the right atrium to about 80-90% of the control value. However, there was no change in the activity of choline acetyltransferase (ChAT) or acetylcholinesterase (AchE), or in the concentration of choline (Ch). Injection of 0.1 mg/kg of digoxin had no significant effect on Ach concentration. When 0.75 and 2.5 mg/kg of digoxin were injected, there was a significant increase in NE concentration in the right atrium. Neither 0.1 nor 0.35 mg/kg caused any changes. Digoxin (0.75 and 2.5 mg/kg) increased heart rate to about 110% of the control values. Thus, high doses of digoxin increase the NE concentration but decrease the Ach concentration in the rat heart, and these changes might be related to functional changes in the autonomic nervous system.

Acetylcholine↗
PubMed1989

Ibopamine vs. digoxin in chronic heart failure: a double-blind, crossover study.

Ibopamine, a dopamine derivative suitable for oral administration, is reported to improve cardiac function in patients with chronic heart failure. In order to evaluate the inotropic effect of ibopamine and to compare it with that of digoxin, we studied 10 patients with chronic heart failure (NYHA II-III). All patients were in sinus rhythm. After a washout period of 5 days, when the patients received a constant diuretic dosage and a placebo, ibopamine 100 mg t.i.d. or digoxin 0.25 mg o.d. was randomly given double-blind. The active treatment was continued for a 10-day period, and was followed by a second washout period of 5 days. Subsequently, the patients received digoxin if previously on ibopamine or ibopamine if previously on digoxin for 10 days. Diuretic was continued at the same dosage throughout the study. At the end of the two washout periods, all patients performed a static (hand grip) and a dynamic exercise (bicycle ergometer). Both ibopamine and digoxin improved cardiac response to both types of exercise compared to the washout periods. In particular, PEP/LVET decreased (p less than 0.001 for both drugs) and O2 consumption improved (from 586 +/- 48 to 716 +/- 35 ml/min for ibopamine and from 585 +/- 38 to 713 +/- 52 ml/min for digoxin). No difference was noted between the two drugs in the improvement of exercise tolerance. No side effects were noted with the two drugs. These data indicate that ibopamine could be a valid alternative to digoxin in heart failure patients in sinus rhythm when given for 10 days. More data are needed to evaluate the long-term efficacy of ibopamine.

Adult↗
PubMed1989

Comparison of digoxin and dobutamine in patients with severe dilatative cardiomyopathy.

The hemodynamic effects of dobutamine were compared with those of digoxin in seven patients with severe diffuse dilatative cardiomyopathy. Dobutamine (7.5 micrograms per kg of body wt per min) was given intravenously for 30 min and then discontinued until hemodynamics returned towards base line. Digoxin (12.5 micrograms per kg) was then given intravenously and hemodynamics were recorded for 120 min. Thereafter, dobutamine was again given at the previous dose. Dobutamine increased cardiac and stroke volume index and decreased pulmonary occlusive (wedge) pressure and systemic vascular resistance without changing heart-rate or arterial pressure. Digoxin also increased cardiac and stroke volume index and decreased pulmonary wedge pressure and systemic vascular resistance with digoxin without changing arterial pressure. In contrast to dobutamine, heart-rate was decreased with digoxin indicating reduced myocardial oxygen demand. Re-infusion of dobutamine did not have any notable hemodynamic effect, with the exception of an increase in heart-rate-systolic pressure production. These data indicate that the positive inotropic properties of digoxin and dobutamine are not additive. Furthermore, concerning the effect of digoxin on the heart-rate, its use seems preferable to the use of sympathomimetic agents such as dobutamine, in patients with diffuse chronic dilatative myocardiopathy.

Aged↗
PubMed1989

Digoxin-like immunoreactive factor in twin and pregnancy-associated hypertensive pregnancies.

The objective of this study was to measure maternal total digoxin-like immunoreactive factor levels in singleton pregnancies with or without hypertension and in twin pregnancies. Plasma digoxin-like immunoreactive factor was measured in 113 third-trimester patients: 51 normotensives, 20 preeclamptics, 19 with latent or chronic hypertension, and 23 with twin pregnancies. The concentration of total digoxin-like immunoreactive factor in the twin gestations (1143 +/- 249 pg/mL) was significantly higher than that in either the normotensive pregnancies (890 +/- 161 pg/mL) (P less than .001) or in the hypertensive pregnancies (903 +/- 256 pg/mL) (P less than .01). However, there were no significant differences in digoxin-like immunoreactive factor levels between the normotensive and hypertensive groups. A trend of higher, although not statistically significant, levels of digoxin-like immunoreactive factor was noted in the chronic hypertensive group as compared with the preeclamptic patients (957 +/- 212 versus 852 +/- 288 pg/mL). We therefore conclude that digoxin-like immunoreactive factor does not contribute significantly to the pathogenesis or prediction of preeclampsia. The increased amount of digoxin-like immunoreactive factor in twin pregnancies may reflect a contribution from multifetal origin, or might be a physiologic adaptive mechanism allowing higher cardiac output by a possible cardiotropic effect.

Adult↗
PubMed1989

Interpretation of elevated postmortem serum concentrations of digoxin in infants and children.

The relationship between excessive postmortem digoxin concentrations (greater than 6.4 nmol/L) and administered dose, and antemortem levels and time of sampling after death were determined in 27 digitalized children who died in our hospital between March 24, 1981 and September 1, 1983. In all 27 cases, postmortem concentrations were higher than antemortem levels (9.5 +/- 2.5 nmol/L and 3.12 +/- 1.72 nmol/L, respectively). In none of these patients was there clinical or electrocardiographic evidence of digitalis toxicity. There was a significant correlation between antemortem and postmortem determinations, and between time of sampling after death and postmortem concentration. Positive correlation existed between antemortem or postmortem concentrations and dose per kilogram. The degree of elevation in digoxin levels was uniform in most cases, and the likelihood of elevation falling in the range 3.5 to 7.0 nmol/L was 66%. If the estimated concentration of digoxin at the time of death was taken as baseline, in 75% of cases the subsequent elevation was between 5.3 and 8.3 nmol/L (mean, 6.5 +/- 1.1 nmol/L). Digoxin concentrations measured in newborn infants not receiving digoxin were significantly higher after death (1.5 +/- 0.3 nmol/L) than in age-matched living infants not receiving digoxin (0.5 +/- 0.3 nmol/L). These data indicate that the size of antemortem dose, the time of sampling after death, and existence of endogenous digoxinlike factors affect postmortem readings of digoxin levels. Consequently, excessive postmortem determinations cannot be directly interpreted as proof of toxic antemortem levels.

Child, Preschool↗
PubMed1989

Effects of compensated heart failure on digoxin pharmacokinetics in cats.

To evaluate the effects of compensated heart failure (HF) on digoxin pharmacokinetic properties in cats, 6 cats with dilated cardiomyopathy were compared with 6 clinically normal (control) cats. Digoxin tablets were administered at a dosage of 0.01 mg/kg of body weight, q 48 h for approximately 10 days, until presumed steady state was reached. Both groups were treated concomitantly with aspirin, furosemide, and a commercial low-salt diet. Retrospectively, control and HF cats were calculated to be at 95% and 97% steady state, respectively. At the time blood samples were collected, HF cats were clinically compensated. Serum digoxin concentration [( DXN]) was determined by radioimmunoassay on samples drawn immediately before and 1, 2, 4, 8, 12, 24, 34, and 48 hours after digoxin administration. Measured and calculated values (peak, 8-hour, and mean [DXN]; elimination half-life [t1/2]; oral clearance; and hours during which [DXN] was in the toxic range) were not significantly different between control and HF cats. To predict individual propensity for digoxin intoxication, serum creatinine and urea concentrations and sulfobromophthalein dye retention were measured in control and HF cats prior to the onset of treatment with digoxin. There was no statistically significant correlation between serum creatinine and urea concentrations when compared with sulfobromophthalein dye retention nor between any of these values and digoxin peak, 8-hour, and mean concentrations or t1/2, oral clearance, or hours during which [DXN] was in the toxic range. Mean serum creatinine and urea nitrogen concentrations were significantly greater (P less than 0.01) and sulfobromophthalein dye retention approached significant prolongation (P less than 0.06) in HF cats, compared with that in control cats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Disposable-column radioimmunoassay for serum digoxin with less interference from metabolites and endogenous digitalis-like factors.

A preparative extraction step using disposable C18 low-pressure chromatography columns greatly improved the specificity of a commercially prepared digoxin radioimmunoassay (RIA). Elution solvents were isopropanol/water (15/85 by vol), which extracted most immunoreactive digitalis-like factors and metabolites, and methanol, which extracted digoxin for RIA. Many different digoxin RIA kits could be used. The coefficients of variation for replicates and duplicates were 4.6% and 5.2%. Analytical recoveries of digoxin standards in serum of 1.0, 0.5, and 0.1 microgram/L were 96%, 95%, and 88%, respectively. Serum digoxin was assayed by this method in 200 patients, 47 of whom were studied by HPLC-RIA. Values correlated better with "true digoxin" by HPLC-RIA (r = 0.93) than did values found by direct assay (r = 0.63). The mean for the isopropanol fraction as a percentage of the mean direct RIA value was higher for the 21 dialysis-dependent patients than was that found for the 179 nondialysis patients (P less than 0.004). The method is suggested as being most useful when metabolites or digitalis-like factors are known to be often high and values for digoxin are disproportionate to the dose.

1-Propanol↗
PubMed1988

Enhancement of digoxin clearance by mannitol diuresis: in vivo studies and their clinical implications.

Because of its narrow margin of safety, digoxin toxicity may occur even during routinely prescribed doses. Due to its very large distribution volume (10 L/kg), only less than 1% of the body load is available for removal, making hemodialysis and hemoperfusion ineffective. Until recently it was assumed that most of the body load of digoxin is eliminated by glomerular filtration. It is now evident that substantial tubular reabsorption and secretion take place. As for the other drugs which are reabsorbed by the tubule (eg Aspirin), we wished to assess whether urine flow rate affect digoxin renal clearance. We studied anesthetized, ventilated dogs. They were preloaded with 25 micrograms/kg IV digoxin the day prior to the experiment. The dogs were infused initially with saline and after a urine collection for digoxin renal clearance 200 ml 10% mannitol were infused over 30 minutes. Digoxin renal clearance was increased 2-3 folds in all cases with a small increase in inulin clearance. Based on these results, the ability of mannitol diuresis to remove significant systemic amounts of digoxin should be tested in acute toxicity in animals. This may be an adjunct modality to FAB antibodies and activated charcoal.

Animals↗
PubMed1986

Interpretation of serum digoxin values in renal failure.

We have studied three circumstances that have been reported to make interpretation of the serum digoxin concentration difficult in patients with renal failure: increased biotransformation; endogenous digitalis-like factors (DLF); and sudden, unexpected increases in serum digoxin values, even after the discontinuation of digoxin. Biotransformation, as estimated by the percent true digoxin in serum, was comparable in patients with renal failure who were dependent on dialysis and in control subjects (76% vs. 73%). Certain commercial immunoassays did not, or rarely, gave values for DLF of clinical significance (greater than 0.2 ng/ml digoxin equivalents) in patients with a wide range of renal dysfunction who were not receiving digoxin. With a sensitive method, values for DLF did not exceed 0.23 ng/ml in 22 dialysis patients dependent on dialysis, but were significantly increased in comparison with values in control subjects. The case histories of two patients with renal failure, acute illness, and sudden unexpected marked increases in serum digoxin concentrations are presented and possible explanations are discussed.

Adult↗
PubMed1986

[Digoxin-propafenone interaction: values and limitations of plasma determination of the 2 drugs. Anti-arrhythmia effectiveness of propafenone].

Propafenon's influence on the pharmacokinetic and actions of digitalis and viceversa have been evaluated in 27 patients (25 with ventricular hyperkinetic arrhythmias and 2 with paroxismal atrial fibrillation). Patients were divided in two groups according to whether the drug firstly administered were digoxin or propafenon. Plasmatic digoxin and/or propafenon's concentrations, these last performed only in 12 patients, were determined before and during the association and after propafenon's interruption at 7.55-9-11 and at 3-8 p.m. During drug's association area under the plasmatic digoxin concentration curve (AUC 12h) increased on the average by 13.8% (from 19.27 +/- 6.002 ng hours/ml to 21.94 +/- 6.198 ng hours/ml: P less than 0.05) and by 19% at the first hour. Neverthless individual behaviour was not homogeneous since the plasmatic digoxin concentration (PDC) increased in 22 cases (81.4%) and decreased in 5 (18.6%). In 6 patients mean increase was 38.8% (from 16.72 +/- 3.0 ng hours/ml to 23.21 +/- 5.44 ng hours/ml) without signs of digoxin intoxication. Another patient with congestive heart failure and basal PDC 1.87 ng/ml experienced digoxin poisoning with fatal ventricular fibrillation after propafenon. Digoxin administration in the second group's patients produced a not significant increase of plasmatic propafenon concentration (PPC). There was a good correlation among propafenon's absolute amount and plasmatic concentration and antiarrhythmic effect and no correlation among PPC and body-weight related dose. Propafenon's to digitalis association induced, in propafenon's steady state, significant P-R longation from 170 to 190 ms (P less than 0.01) but HR, QRS and QTc didn't show any important change (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Digoxin inactivation by the gut flora in infancy and childhood.

Inactivation of digoxin by reduction of the lactone ring has recently been shown to occur in one third of adults and to be mediated by anaerobic intestinal bacteria. Children from birth through adolescence were studied to determine the pattern of development of this gut flora-mediated process. None of 36 digitalized infants 8 months of age or less excreted reduced digoxin metabolites in the urine. The adult pattern of digoxin reduction product excretion by one third of patients was observed after 16 months of age; however, high levels of digoxin reduction products such as are found in 10% of adults were not encountered in children less than 9 years of age. Even though reduced metabolites were not formed in vivo early in life, stool cultures of 20 of 73 infants younger than 8 months of age contained digoxin reduction product-forming bacteria at high concentrations, in some instances as early as the second week of life. Maturation of the gut flora with respect to digoxin metabolism appears to be a protracted process. The relative digoxin resistance of infants and children is not due to bacterial inactivation.

Adolescent↗
PubMed1987

Pharmacokinetic prediction of serum digoxin concentration in the elderly.

The usefulness of pharmacokinetic predictions of serum digoxin concentrations was evaluated in a group of 19 elderly residents of a nursing home. A statistically significant correlation between the calculated and measured digoxin level was found with a 95% confidence limit of 0.55 ng/mL (0.7 nmol/L). Although the use of liquid-filled digoxin capsules and the utilization of the equations described in this article resulted in improved predictability of steady-state serum digoxin concentrations, the calculated serum digoxin level significantly underestimated the measured value in 33% of the patients who were not receiving any medications known to increase serum digoxin concentration. Further studies are needed to improve the reliability of pharmacokinetic models in estimating serum digoxin concentrations in the elderly.

Aged↗
PubMed1986

Clinical utility of serum digoxin level tests in hospitalized elderly patients.

To assess the clinical utility of serum digoxin tests in the elderly and to ascertain the use by physicians of test results, digoxin levels were obtained from 77 consecutive, elderly patients (means age 72 years) taking digoxin on admission to a rehabilitation hospital. Blood samples were drawn the morning following admission (prior to the administration of digoxin) and were repeated in two weeks. Signs or symptoms of digoxin toxicity were seen in all 13 patients with levels above the therapeutic range. Of 38 patients with therapeutic levels, 16 had signs or symptoms compatible with underdigitalization or digoxin toxicity. Physicians were significantly more likely to respond to both the initial and follow-up serum digoxin test result when the first test result was above the therapeutic range.

Adult↗
PubMed1985

Quinidine-digoxin interaction: are the pharmacokinetics of both drugs altered?

An open randomized crossover trial to investigate quinidine-digoxin interactions under steady-state conditions with special attention to quinidine pharmacokinetics was performed in 6 healthy male volunteers. Coadministration of quinidine sulphate induces a prolongation of digoxin elimination half-life (means +/- SD) from 33.0 +/- 8.0 to 43.9 +/- 6.2 hours, causing an augmentation of 0/48 AUC (means +/- SD) from 37.8 +/- 14.1 to 100.2 +/- 30.4 ng/ml.h. This increase in serum digoxin concentration-time course was caused by a decrease of both renal clearance (means +/- SD) from 150.7 +/- 46.5 to 79.0 +/- 23.3 ml/min and of minor importance, total clearance (means +/- SD) from 198.8 +/- 66.4 to 91.7 +/- 21.9 ml/min. A decrease in apparent volume of distribution of digoxin (means +/- SD) from 520.1 +/- 115.2 to 344.5 +/- 78.2 l could also be observed: When digoxin was given additionally, two quinidine-pharmacokinetic parameters were altered: renal quinidine clearance decreased from (means +/- s) 61.2 +/- 11.5 to 45.7 +/- 13.7 ml/min, causing a prolongation of elimination half-life of quinidine (means +/- s) from 10.34 +/- 1.76 to 12.28 +/- 1.23 hours. These altered parameters induced an augmentation in 0/48 AUC of quinidine of 11% on the average but this change was not statistically significant because of the relatively large standard-deviation in serum quinidine concentrations. Considering the reduction of renal digoxin clearance, the mechanism mainly responsible for the quinidine-digoxin interaction, the decrease in renal quinidine clearance, appears to be most remarkable as well.

Acetyldigoxins↗
PubMed1979

[Behavior of the plasma level of digoxin in the rat in induced experimental hyperreninemia].

PRA, plasma and urine aldosterone levels and plasma digoxin were measured in rats in which digoxin had been administered under conditions of high PRA and high aldosterone levels experimentally induced by administering distilled water load and in rats in which digoxin had been administered without distilled water load. Results show that under conditions of high PRA and high aldosterone levels, plasma digoxin concentrations as measured 6 h after treatment were higher (45,3%) than in rats having received digoxin without water load. In assays carried out on rats sacrificed 12 h after digoxin treatment (with or without water load) all values approach basic levels again, thus suggesting that in rats too aldosterone might compete with digoxin at the level of tubular excretion.

Aldosterone↗
PubMed1985

Effect of an aminocardenolide and digoxin upon atrioventricular refractory period in the dog.

The ability of digoxin and a 4-aminocardenolide, ASI-222, to alter atrioventricular nodal refractory period (AVRP) was determined as a function of the maximum subarrhythmic dose (MSAD) in the dog anesthetized with morphine-pentobarbital. ASI-222, a highly polar and potent inhibitor of Na+, K+-adenosine triphosphatase produces a cardiotoxicity in dogs prominently involving atrioventricular nodal blockade rather than ventricular premature ectopic beats and tachycardia seen with digoxin. AVRP was assessed with trains of electrically isolated stimuli of decreasing pulse interval delivered to the right atria. Digoxin and ASI-222 were infused i.v. at rates which produced cardiac arrhythmias in about 100 min in dogs either: 1) with intact nerves, 2) pretreated with atropine, 3) without reflex receptors (without vagus and carotid sinus nerves, 4) without cardiac sympathetic nerves and adrenals or 5) pretreated with metoprolol. In dogs with intact nerves, ASI-222 produced greater increases in AVRP than digoxin at fractions of the MSAD; however, both glycoside produced a similar elevation at the MSAD (approximately equal to 30% increase). Atropine did not alter the AVRP response to ASI-222 but prevented the lengthening due to digoxin except for that which occurred near the MSAD. Removal of reflex receptor afferents (and vagi) had an effect similar to atropine on the AVRP response to digoxin, but completely prevented any response to ASI-222. Prior sympathectomy or beta adrenergic blockade abolished the AVRP response to ASI-222 but did not alter the responses to digoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

[Digitalis therapy in practice: correlation between clinical evaluation and plasma digoxin concentration (author's transl)].

In a prospective study 73 patients on maintenance digitalis treatment at the Paracelsus Institute, Bad Hall, were clinically examined and the dosage of the drug was adjusted according to cardiac symptoms. The clinical effects were correlated to digoxin concentrations measured on the day following admission to hospital and on the 21st day of treatment. The following practical conclusions were reached: 1. More than 50% of the patients were underdigitalized. 2. There is often no indication for digitalis therapy in patients with a low daily maintenance digoxin dosage and normal renal funciton. 3. The usual recommended maintenance dosage of digoxin provides serum digoxin levels in the lower region of the therapeutic range. 4. Patients with symptoms of decompensation taking an average dosage of digoxin need more digitalis. There is generally no danger of toxicity when the dosage is increased. 5. The serum digoxin concentration in patients with slightly reduced renal function lies in the upper region of the therapeutic range with usual doses of digoxin.

Arrhythmias, Cardiac↗
PubMed1979

[Radioimmunologic determination of serum digoxin. Methodological and 1st clinical experiences].

The tested quality signs of the digoxin-RIA (Medica) correspond to other RIA-test methods. The digoxin-RIA (Medica) is, therefore, well suited for clinical examinations. In the dilanacin- (digoxin-) long-term therapy with the maintenance dose of 0.5 mg digoxin a day 75.4% of the patients examined (n = 65) were within the therapeutic field. In each case 12.3% were underdigitalised or overdigitalised, respectively. In the 8 patients in the toxic region only the half showed signs of digoxin intoxication. It is referred to the importance of creatinine and potassium in the serum, the digoxin clearance depending on age, the body weight and the body surface, respectively, in very obese patients for the height of the serum digoxin level and for the compatibility of this heart glycoside.

Aged↗