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Lanoxin (Digoxin)

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Lanoxin is an effective medication which is used in treatment of certain types of fast heartbeats such as atrial fibrillation or fluttering arrhythmia and heart failure. It also treats angina. This drug can also be used after heart attack.

Other names for this medication:

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Also known as:  Digoxin.


Lanoxin target is struggle against certain types of fast heartbeats such as atrial fibrillation or fluttering arrhythmia and heart failure. It is also treats angina. This drug can also be used after heart attack. The effectiveness of Lanoxin is in keeping the heart rhythm under control and to make heart work better (regularly and strongly). It is cardiac (or digitalis) glycosides.

Generic name of Lanoxin is Digoxin.

Lanoxin is also known as Digoxin, Digitalis, Digitek, Lanoxicaps.

Brand names of Lanoxin are Lanoxicaps, Lanoxin, Cardoxin, Digitek, Lanoxin Elixir Pediatric.


Take Lanoxin tablets (0.25 mg), capsules and pediatric elixir (liquid) orally.

Elderly people (> 65 years) should take the lowest dose.

Take Lanoxin at the same time once a day with water.

Do not crush or chew it.

If you want to achieve most effective results do not stop taking Lanoxin suddenly.


If you overdose Lanoxin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Lanoxin overdosage: confusion, irregular heartbeats, nausea, seizures, vomiting, extremely fast or slow heartbeats, hallucinations, tiredness, problems with vision, diarrhea, lack of appetite.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Lanoxin are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Lanoxin if you are allergic to Lanoxin components.

Do not take Lanoxin if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Lanoxin if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Lanoxin in case of taking medicines as a steroid medicine (prednisone (such as Deltasone), methylprednisolone (such as Medrol), prednisolone (such as Prelone, Pediapred), dexamethasone (such as Decadron)); a cancer chemotherapy drug; amphotericin B (such as Fungizone); indomethacin (such as Indocin); rifampin (such as Rifadin, Rimactane); cholestyramine (such as Questran, Prevalite) or colestipol (such as Colestid); a thyroid medication; a beta-blocker (atenolol (such as Tenormin), propranolol (such as Inderal), acebutolol (such as Sectral), metoprolol (such as Lopressor), carteolol (such as Cartrol), labetalol (such as Normodyne, Trandate) or nadolol (such as Corgard)); a diuretic (hydrochlorothiazide (such as HCTZ, HydroDiuril, others), chlorothiazide (such as Diuril), chlorthalidone (such as Hygroton, Thalitone), furosemide (such as Lasix), torsemide (such as Demadex), bumetanide (such as Bumex), ethacrynic acid (such as Edecrin), triamterene (such as Dyrenium, Maxzide, Dyazide), amiloride (such as Midamor), spironolactone (such as Aldactone), eplerenone (such as Inspra)); metoclopramide (such as Reglan); tetracycline (such as Broadspec, Emtet, Panmycin, Sumycin, Tetracap); erythromycin (such as E.E.S., E-Mycin, Eryc, Ery-Tab, PCE) or clarithromycin (such as Biaxin); sulfasalazine (such as Azulfidine); sulfasalazine (such as Azulfidine); another medicines for irregular heartbeats (quinidine (such as Quinidex, Quinora, Cardioquin), amiodarone (such as Cordarone) or propafenone (such as Rythmol)); itraconazole (such as Sporanox); a calcium channel blocker (diltiazem (such as Cardizem, Dilacor XR, Tiazac), amlodipine (such as Norvasc), felodipine (such as Plendil), nifedipine (such as Procardia, Adalat), verapamil (such as Verelan, Calan, Isoptin, Covera-HS)), an antacid or laxative that contains aluminum, magnesium or kaolin-pectin (such as Maalox, Rolaids, Mylanta, Milk of Magnesia).

Be careful with Lanoxin if you have allergies to medicines, foods, or other substances.

Be careful with Lanoxin if you suffer from or have a history of thyroid disease, cancer, kidney disease, heart arrhythmias.

Use Lanoxin with great care in case you want to undergo an operation (dental or any other).

Elderly people (> 65 years) should take the lowest dose.

Avoid alcohol.

Avoid machine driving.

Do not stop taking Lanoxin suddenly.

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Etanercept, a soluble recombinant human tumor necrosis factor receptor (TNFr), is effective and well tolerated in the treatment of rheumatoid arthritis, juvenile rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and psoriasis. The primary objective of this study was to investigate the potential pharmacokinetic and pharmacodynamic interaction between digoxin and etanercept at steady state. In a crossover, open-label, nonrandomized, 3-period study, 12 healthy male subjects received loading oral doses of digoxin 0.5 mg every 12 hours on day 1 and 0.25 mg every 12 hours on day 2, followed by a daily maintenance dose of 0.25 mg for a total of 27 days. Etanercept was administered as a twice-weekly 25-mg subcutaneous dose beginning on day 9 and continuing up to day 37 for a total of 9 doses. All ratios of maximum plasma concentration (C(max)) and area under the plasma concentration versus time curve (AUC) for pharmacokinetics of digoxin fell within the confidence interval of 0.8 to 1.25. Although not considered clinically relevant, the mean C(max) and AUC of etanercept were 4.2% and 12.5% lower, respectively, when etanercept was given with digoxin than when administered alone. There were no clinically relevant changes in the electrocardiogram (ECG) parameters, and adverse events did not increase when both drugs were combined. In conclusion, there is no clinically relevant interaction between etanercept and digoxin, and both drugs can be safely coadministered without the need for a dosage adjustment.

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Acute pseudo-obstruction of the colon (Ogilvie's syndrome) is a rare but potentially morbid complication of burn injury. Two thousand seven hundred three consecutive critically ill patients with burns were reviewed for findings consistent with pseudo-obstruction. Eight (0.29%) patients were identified. Mean age was 63.5 years, and mean burn size was 24.6% total body surface area. All patients were undergoing mechanical ventilation at the time of diagnosis. Six had a previous cardiac condition or complication, and five were on digoxin. Diagnosis was suspected in seven patients before colonoscopy or surgery. Six patients were treated with colonoscopy alone with one treatment failure. Two deaths occurred during hospitalization. Two late deaths were due to underlying cardiac conditions. The preferred treatment of Ogilvie's syndrome is nasogastric suction, colonic decompression, and close observation with surgery reserved for treatment failures or when diagnosis is in doubt. The incidence of Ogilvie's syndrome in patients with burns appears to be related to nonburn medical conditions, especially cardiopulmonary complications and age, rather than to the burn itself.

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Placental ATP binding cassette (ABC) transporters protect placental and fetal tissues by effluxing xenobiotics and endogenous metabolites. We have investigated the effects of cytokines and survival/growth factors, implicated in various placental pathologies, on ABC transporter expression and function in primary placental trophoblast cells. Treatment of primary term trophoblasts in vitro with tumor necrosis factor-alpha (TNF-alpha) or interleukin (IL)-1beta decreased mRNA and protein expression of apical transporters ABCB1/multidrug resistance gene product 1 (MDR1) and ABCG2/breast cancer resistance protein (BCRP) protein by 40 to 50% (P < 0.05). In contrast, IL-6 increased mRNA and protein expression of the basolateral transporter ABCB4/MDR3 (P < 0.05), whereas ABCC1/MRP1 expression was unaltered. Pretreatment of trophoblasts with TNF-alpha over 48 h resulted in significantly decreased BCRP efflux activity (increased mitoxantrone accumulation) with minimal changes in MDR1/3 activity. Epidermal growth factor (EGF) and insulin-like growth factor II, on the other hand, significantly increased BCRP expression at the mRNA and protein level (P < 0.05); EGF treatment also increased BCRP functional activity. Estradiol stimulated BCRP, MDR1, and MDR3 mRNA and protein expression by 40 to 60% and increased MDR1/3 functional activity (P < 0.05). Progesterone had modest positive effects on MRP1 mRNA and MDR1 protein expression (P < 0.05). In conclusion, this study shows that proinflammatory cytokines, sex steroids, and growth factors exert independent effects on expression of apical and basolateral placental ABC transporters in primary trophoblast. Such changes could alter placental drug disposition, increase fetal susceptibility to toxic xenobiotics, and impact on placental viability and function.

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Troglitazone is a new thiazolidinedione oral antidiabetic agent approved for use to improve glycaemic control in patients with type 2 diabetes. It is rapidly absorbed with an absolute bioavailability of between 40 and 50%. Food increases the absorption by 30 to 80%. The pharmacokinetics of troglitazone are linear over the clinical dosage range of 200 to 600 mg once daily. The mean elimination half-life ranges from 7.6 to 24 hours, which facilitates a once daily administration regimen. The pharmacokinetics of troglitazone are similar between patients with type 2 diabetes and healthy individuals. In humans, troglitazone undergoes metabolism by sulfation, glucuronidation and oxidation to form a sulfate conjugate (M1), glucuronide conjugate (M2) and quinone metabolite (M3), respectively. M1 and M3 are the major metabolites in plasma, and M2 is a minor metabolite. Age, gender, type 2 diabetes, renal impairment, smoking and race do not appear to influence the pharmacokinetics of troglitazone and its 2 major metabolites. In patients with hepatic impairment the plasma concentrations of troglitazone, M1 and M3 increase by 30%, 4-fold, and 2-fold, respectively. Cholestyramine decreases the absorption of troglitazone by 70%. Troglitazone may enhance the activities of cytochrome P450 (CYP) 3A and/or transporter(s) thereby reducing the plasma concentrations of terfenadine, cyclosporin, atorvastatin and fexofenadine. It also reduces the plasma concentrations of the oral contraceptive hormones ethinylestradiol, norethindrone and levonorgestrel. Troglitazone does not alter the pharmacokinetics of digoxin, glibenclamide (glyburide) or paracetamol (acetaminophen). There is no pharmacodynamic interaction between troglitazone and warfarin or alcohol (ethanol). Pharmacodynamic modelling showed that improvement in fasting glucose and triglyceride levels increased with dose from 200 to 600 mg. Knowledge of systemic troglitazone exposure within a dose group does not improve the prediction of glucose lowering response or adverse effects beyond those based on the administered dose.

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To describe the clinical presentation, diagnosis, and contemporary treatment of chronic heart failure (CHF) while emphasizing the important role of the pharmacist.

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CaViar reported spontaneous and paced APs and CTs with high signal-to-noise ratio and low phototoxicity. Quinidine, flecainide, E-4031, digoxin and cisapride prolonged APs, while verapamil and nifedipine shortened APs. Early after depolarizations (EADs) were elicited by quinidine, flecainide and cisapride. All but four compounds (amiodarone, chromanol, nifedipine, verapamil) prolonged AP rise time. Nifedipine and verapamil decreased CT amplitude, while digoxin increased CT amplitude. Pentamidine prolonged APs after chronic exposure.

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Parasympathetic nerves to the atrioventricular node were stimulated from the proximal coronary sinus as well as the posteroseptal right atrium. Stimulation at the posteroseptal right atrium resulted in the greatest response, and digoxin enhanced this response. The augmented response suggests that an interaction may exist between parasympathetic stimulation and digoxin at the end organ.

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We examined the relationship between the excretion of electrolytes (sodium, potassium and calcium), dopamine and digoxin-like immunoreactive substance in 41 young healthy female subjects (age 18-23 years) in order to study the interaction of electrolyte intake on dopamine and digoxin-like immunoreactive substance--factors which have been postulated to have a pathogenic role in hypertension. Sodium excretion was significantly correlated with dopamine excretion (r = 0.545, P < 0.0005) and digoxin-like immunoreactive substance (r = 0.359, P < 0.02). There was also a significant correlation between calcium and digoxin-like immunoreactive substance (r = 0.345, P < 0.03). Stepwise multiple regression analysis further confirmed that sodium is the only contributor to dopamine excretion and calcium is the only contributor to digoxin-like immunoreactive substance (r2 = 0.114). We conclude that in young healthy subjects dopamine excretion is determined partly by sodium intake and that the excretion of digoxin-like immunoreactive substance is independent of sodium intake.

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Bosentan, a dual endothelin receptor antagonist, is indicated for the treatment of patients with pulmonary arterial hypertension (PAH). Following oral administration, bosentan attains peak plasma concentrations after approximately 3 hours. The absolute bioavailability is about 50%. Food does not exert a clinically relevant effect on absorption at the recommended dose of 125 mg. Bosentan is approximately 98% bound to albumin and, during multiple-dose administration, has a volume of distribution of 30 L and a clearance of 17 L/h. The terminal half-life after oral administration is 5.4 hours and is unchanged at steady state. Steady-state concentrations are achieved within 3-5 days after multiple-dose administration, when plasma concentrations are decreased by about 50% because of a 2-fold increase in clearance, probably due to induction of metabolising enzymes. Bosentan is mainly eliminated from the body by hepatic metabolism and subsequent biliary excretion of the metabolites. Three metabolites have been identified, formed by cytochrome P450 (CYP) 2C9 and 3A4. The metabolite Ro 48-5033 may contribute 20% to the total response following administration of bosentan. The pharmacokinetics of bosentan are dose-proportional up to 600 mg (single dose) and 500 mg/day (multiple doses). The pharmacokinetics of bosentan in paediatric PAH patients are comparable to those in healthy subjects, whereas adult PAH patients show a 2-fold increased exposure. Severe renal impairment (creatinine clearance 15-30 mL/min) and mild hepatic impairment (Child-Pugh class A) do not have a clinically relevant influence on the pharmacokinetics of bosentan. No dosage adjustment in adults is required based on sex, age, ethnic origin and bodyweight. Bosentan should generally be avoided in patients with moderate or severe hepatic impairment and/or elevated liver aminotransferases. Ketoconazole approximately doubles the exposure to bosentan because of inhibition of CYP3A4. Bosentan decreases exposure to ciclosporin, glibenclamide, simvastatin (and beta-hydroxyacid simvastatin) and (R)- and (S)-warfarin by up to 50% because of induction of CYP3A4 and/or CYP2C9. Coadministration of ciclosporin and bosentan markedly increases initial bosentan trough concentrations. Concomitant treatment with glibenclamide and bosentan leads to an increase in the incidence of aminotransferase elevations. Therefore, combined use with ciclosporin and glibenclamide is contraindicated and not recommended, respectively. The possibility of reduced efficacy of CYP2C9 and 3A4 substrates should be considered when coadministered with bosentan. No clinically relevant interaction was detected with the P-glycoprotein substrate digoxin. In healthy subjects, bosentan doses >300 mg increase plasma levels of endothelin-1. The drug moderately reduces blood pressure, and its main adverse effects are headache, flushing, increased liver aminotransferases, leg oedema and anaemia. In a pharmacokinetic-pharmacodynamic study in PAH patients, the haemodynamic effects lagged the plasma concentrations of bosentan.

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Twenty-six patients having received digoxin and clarithromycin concurrently during their hospital stay were included in the study. Of these, 12 patients (46.2%) had serum digoxin concentrations above the therapeutic range: 7 received digoxin in doses unsuited for their age and/or renal function, and 2 fell short of the mean period of time considered adequate for an interaction to occur. Therefore, only 3 patients had serum digoxin concentrations above the therapeutic range, probably because of an interaction with clarithromycin, and all three had digitalis intoxication symptoms.

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Heart failure (HF) is a major cause of mortality and morbidity and one of the most frequent reasons for hospital admission in the United States and Europe. Currently, more than 50% of HF patients have a normal (N) left ventricular (LV) ejection fraction (EF) (LVEF >50%). The main pathophysiologic processes involved in HFNEF are increased LV stiffness and abnormal relaxation, resulting in impaired LV filling. Hypertension and myocardial ischemia are the most common causes of HFNEF. Precipitating factors include volume overload, tachycardia, physical exercise, systemic stressors (such as fever and infection), arrhythmia, increased salt intake, and use of nonsteroidal anti-inflammatory drugs. There is little evidence to guide treatment, as previously HFNEF patients have been excluded from clinical trials on the basis of a normal LVEF. Survival improved over time in patients with reduced (R) EF (HFREF) (LVEF <40%), reflecting the beneficial effects of treatment in this phenotype. However, survival did not improve for HFNEF patients. The approach to the treatment of HFNEF patients should focus on reducing LV filling pressure, controlling hypertension, modifying ischemia, and improving LV relaxation. Therefore, diuretics are suitable for HFNEF patients to reduce ventricular filling pressure. Hypertension can be treated by using multiple agents if necessary. Drugs of particular interest and recommended to treat hypertension are calcium channel blockers (CCBs) and antagonists of the renin-angiotensin-aldosterone system, such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and aldosterone antagonists. Ischemic heart disease can be treated with antiplatelet therapy, anticoagulants, and β-blockers. Heart rate control in atrial fibrillation can be achieved with β-blockers and digoxin. Finally, ACE inhibitors and ARBs could potentially decrease LV hypertrophy in hypertensive patients with HFNEF.

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This is the first study demonstrating changes of Na+/K(+) -ATPase molecules not only in enzyme activity, but also on protein level. Our results might contribute to the understanding of the resistance of neonatal cell membranes toward the pharmacodynamic actions of cardiac glycosides.

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The beneficial effects of digoxin on common clinical end points in patients with HF were similar, regardless of SDC.

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We included 235 routine monitoring and clinical laboratory test data (steady-state serum digoxin concentration and Ccr values), obtained from hospitalized patients receiving digoxin for treatment of congestive heart failure. The 107 data sets were fitted to a hyperbolic model to account for the relation between the ratio of serum digoxin level to the daily dose (L/D) and the Ccr values determined by six methods. Their correlation coefficients (r) were computed by non-linear regression analysis. To evaluate the validity of the best-fitting model, the predictive performance of the L/D ratios was compared with those given by seven reference models previously published, using another 128 data sets.

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Before electric conversion, all treatments significantly decreased mean heart rate. Spontaneous conversion to sinus rhythm was achieved in 6% of patients of group A (3 of 46) versus 25% of group B (11 of 44) and 3% (1 of 30) of group C (A/C vs B, P < .005). Current conversion was more successful in group B (91%) compared with group A (76%) and group C (67%) (B vs A/C, P < .05), with no difference in the electric threshold for effective conversion (P = not significant). At the 24-hour time point, early relapse of atrial fibrillation was similar between groups A and B (A, 2%; B, 3%; P = not significant) and lower than group C (12%) (P < .01), whereas at the 1-month time point the recurrence rate was lower in group B (28%) versus groups A (56%) and C (78%) (B vs A/C, P < .01). No significant side effects were reported.

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A prospective, controlled, randomized study of 80 patients undergoing esophageal operations was undertaken, in which one group of patients was given digoxin and the other was not. The incidence of cardiac dysrhythmia was compared in each group. Twenty-six patients underwent operation for benign disease. Equal numbers were digitalized or not and no dysrhythmias occurred. Fifty-four patients underwent operation for malignant disease. Of 26 in the group digitalized, 12 suffered dysrhythmia (46%). Of 28 not digitalized, 9 suffered dysrhythmia (32%). Overall, 39% of patients with malignant disease suffered a dysrhythmia compared with none with benign disease (p < 0.002 by chi 2).

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It can be concluded that poor glycemic control evokes greater reduction in erythrocyte Na+K+-ATPase activity and promote enzyme-blood atherogenic lipid relationships in Type 1 diabetic Nigerian patients.

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The potential mutual interaction between cerivastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, and digoxin was assessed in this nonmasked, nonrandomized, multiple-dose study. The effect of cerivastatin 0.2 mg on mean plasma digoxin levels and the effect of digoxin on the single-dose pharmacokinetics of cerivastatin were assessed in 20 healthy normocholesterolemic men between 18 and 45 years of age weighing 140 to 200 lbs (63.3 to 90.0 kg). Subjects were given a single dose of cerivastatin 0.2 mg. After a 2-day washout period, subjects were given a loading dose of digoxin 0.5 mg for 3 days followed by 0.25 mg daily for 5 additional days (period 1-digoxin alone). Concurrent dosing with cerivastatin 0.2 mg continued for 14 days (period 2-digoxin and cerivastatin), followed by an 8-day course of digoxin-only administration and an optional 6-day extension of digoxin-only treatment for a total of 14 days (period 3). Safety was assessed through physical examination, electrocardiography, laboratory tests, and ophthalmologic examination. Ratio analyses of mean digoxin plasma trough levels, 24-hour urinary digoxin levels, and digoxin clearance with and without concurrent cerivastatin dosing also were carried out. In addition, single-dose pharmacokinetic variables for cerivastatin, including area under the curve (AUC(0-24)), peak concentration (C(max)), time to peak concentration (T(max)), and elimination half-life (t1/2), were examined with and without concurrent digoxin dosing. Eleven of the 20 subjects completed the entire study. Seven subjects discontinued the study because of treatment-emergent adverse events or laboratory abnormalities that were mostly unrelated to cerivastatin, and 2 subjects were discontinued because of protocol violations. Treatment-emergent adverse events developed in 12 subjects receiving cerivastatin; 11 of these subjects were receiving digoxin concurrently. Six adverse events that led to discontinuation of treatment were unrelated to cerivastatin but were related to digoxin or to a preexisting condition. The most commonly reported event was headache, which occurred with equal frequency compared with placebo groups in large cerivastatin clinical trials. Other events were mild or moderate and resolved without intervention. Mild and transient elevations in hepatic transaminase and creatine kinase values (all <2 times the upper limit of normal) were observed in 7 subjects. After 14 days of concurrent dosing of cerivastatin and digoxin, steady-state digoxin plasma levels, urinary digoxin levels, and urinary digoxin clearance were unchanged compared with steady-state digoxin levels when digoxin was given alone. Compared with dosing with digoxin alone, the AUC(0-24), Cmax, and t1/2 for cerivastatin increased 3%, 20%, and 7%, respectively, while the T(max) was reduced by 18% during concurrent treatment with digoxin. These changes are minimal and would not be expected to be clinically relevant. These results demonstrate that when cerivastatin is administered concurrently with digoxin, neither digoxin nor cerivastatin plasma levels are altered. The combination therapy was generally well tolerated.

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The present study was undertaken to evaluate cardiotonic activity of aqueous extract of heartwood of P. marsupium. This plant species contains 5,7,2-4 tetrahydroxy isoflavone 6-6 glucoside which are potent antioxidant and are believed to prevent cardiovascular diseases. Cardiotonic effect of aqueous extract of heartwood of P. marsupium was studied by using isolated frog heart perfusion technique (IFHP). Calcium free Ringer solution was used as vehicle for administration of aqueous extract of P. marsupium as a test extract and digoxin as a standard. A significant increase in height of force of contraction (positive inotropic effect) and decrease in heart rate (negative chronotropic effect) at a very low concentration (0.25 mg/ml) was observed with test extract as compared to the same dose of a standard digoxin. The present results indicated that a significant increase in height of force of contraction with decrease in heart rate was observed as the dose of test extract increased. The test extract produced cardiac arrest at 4 mg/ml, a higher concentration, as compared to standard, digoxin (0.5 mg/ml). Compared to digoxin, a drug with narrow therapeutic window, P. marsupium showed wide therapeutic window.

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Serum pentosidine concentration is an independent prognostic factor for heart failure, and this new marker may be useful for risk stratification of patients with heart failure. Patients were divided into 4 groups based on the serum pentosidine levels.

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lanoxin drugs 2017-11-10

The allelic variants in buy lanoxin the human MDR1 gene are likely to be associated with altered absorption and/or disposition profiles of digoxin and P-glycoprotein-mediated drug interaction

lanoxin tablets 2016-12-15

The effect of digoxin administration on the serum concentration of the cardiac troponin I (cTnI) has not been reported to date in equidae. This study was therefore designed to evaluate the effect of digoxin on cardiac cell damage in donkeys (Equus asinus) as assessed by cTnI, acid-base and buy lanoxin electrolyte balance and haematobiochemical profiles. Ten clinically healthy donkeys were given an IV infusion of digoxin at a dose of 14 μg/kg. Blood samples were collected from the donkeys up through 72 h post-injection.

lanoxin prices 2017-11-16

Rate control is less costly and buy lanoxin more effective than rhythm control and should be the initial treatment for atrial fibrillation among patients with coexisting heart failure.

lanoxin tablet composition 2016-01-20

Digoxin is a well-known probe for the activity of P-glycoprotein. The objective of this work was to apply different methods for covariate selection in non- buy lanoxin linear mixed-effect models to study the relationship between the pharmacokinetic parameters of digoxin and the genotype for two major exons located on the multi-drug-resistance 1 (MDR1) gene coding for P-glycoprotein.

lanoxin 125 mg 2017-06-06

A cohort study of CTS patients at Hartford Hospital was undertaken to evaluate whether Hispanic patients had a lower incidence of post-CTS AF than Caucasians. First, Hispanic patients were compared to the total Caucasian population. Then differences in important baseline predictors of AF were probed between groups. Finally, Hispanic patients undergoing CTS were matched (1:4 matching buy lanoxin ) with Caucasian patients based upon known predictors of post-CTS AF including age >70 years, valvular surgery, AF history, previous CTS, peripheral vascular disease, gender, pre-CTS digoxin and beta-blocker intolerance.

lanoxin medication 2015-01-08

The relationship of SCD to new-onset AF was evaluated in 8831 hypertensive patients with electrocardiographic left ventricular hypertrophy with no history of AF, in sinus rhythm on their baseline electrocardiogram, randomly assigned to losartan- or atenolol-based treatment. During 4.7±1.1 years mean follow-up, new-onset AF occurred in 701 patients (7.9%) and SCD in 151 patients (1.7%). In univariate Cox analyses, new-onset AF was associated with a >4-fold higher risk of SCD (hazard ratio, buy lanoxin 4.69; 95% CI interval, 2.96-7.45; P<0.001). In multivariate Cox analyses adjusting for age, sex, race, diabetes mellitus, history of heart failure, myocardial infarction, ischemic heart disease, stroke, smoking, serum high-density lipoprotein cholesterol, creatinine, glucose, and urine albumin/creatinine ratio as standard risk factors, and for incident myocardial infarction, in-treatment use of digoxin, systolic and diastolic pressure, heart rate, QRS duration, Cornell voltage-duration product, and Sokolow-Lyon voltage left ventricular hypertrophy treated as time-varying covariates, new-onset AF remained associated with a >3-fold increased risk of SCD (hazard ratio, 3.13; 95% confidence interval, 1.87-5.24; P<0.001).

lanoxin mg 2015-01-30

Sixteen healthy men and women volunteers buy lanoxin .

lanoxin normal dose 2017-09-04

After a single oral dosing, madecassoside was widely distributed in heart, liver, spleen, lung and kidney of rats, and the levels of madecassoside in liver and kidney were relatively higher than other organs. The excretions of madecassoside in bile, urine and feces were 7.16% (0-12 h), 0.25% (0-72 h) and 24.68% (0-72 h), respectively. The findings suggested that madecassoside might excrete mainly by metabolites. The combination with either digoxin or probenecid significantly attenuated the buy lanoxin excretion of madecassoside as parent from bile, indicating that P-glycoprotein and multidrug resistance-associated protein might contribute to the hepatobiliary elimination of madecassoside. The presence of enterohepatic circulation, as implied by double-humped profiles in plasma and tissue concentration-time curves, was confirmed by a linked-rat model. Furthermore, three metabolities of madecassoside were indentified in rat feces and the possible metabolic pathways were proposed.

lanoxin dosage tablets 2015-03-19

ORM-10962 significantly reduced the inward/outward NCX currents with estimated EC50 values of 55/67 nM, respectively. The compound, even at a high concentration of 1 μM, did not modify significantly the magnitude of ICaL in CMs, neither had any apparent influence buy lanoxin on the inward rectifier, transient outward, the rapid and slow components of the delayed rectifier potassium currents, the late and peak sodium and Na+/K+ pump currents. NCX inhibition exerted moderate positive inotropic effect under normal condition, negative inotropy when reverse, and further positive inotropic effect when forward mode was facilitated. In dog Purkinje fibres 1 μM ORM-10962 decreased the amplitude of digoxin induced delayed afterdepolarizations (DADs). Pre-treatment with 0.3 mg/kg ORM-10962 (i.v.) 10 min before starting ouabain infusion significantly delayed the development and recurrence of ventricular extrasystoles (by about 50%) or ventricular tachycardia (by about 30%) in anesthetized guinea pigs. On the contrary, ORM-10962 pre-treatment had no apparent influence on the time of onset or the severity of I/R induced arrhythmias in anesthetized rats and in Langendorff perfused guinea-pig hearts.

lanoxin drug card 2017-02-09

In the multivariate model, left ventricular diameter (LVDs)-index (P buy lanoxin =0.0067), presence of pulmonary oedema on radiography (P=0.043), presence of ventricular premature complexes (VPCs) (P=0.0012), higher plasma creatinine (P=0.0002), lower plasma protein (P=0.029) and great Dane breed (P=0.0003) were negatively associated with survival. Most dogs were treated with angiotensin-converting enzyme inhibitors (93%) or furosemide (86%), and many received digoxin (50%) and/or pimobendan (30%). Thirteen dogs were lost to follow-up. No conclusions could be made in this study on the association between use of drugs and survival.

lanoxin 2 mg 2017-03-12

It was concluded that both enzyme-linked chemiluminescent immunosorbent and turbidimetric digoxin assays buy lanoxin are free from ginseng interferences.

lanoxin pill identifier 2016-08-06

Voclosporin 0.4 mg kg(-1) was administered to 24 subjects in each of five studies, as follows: every 12 h (Q12H) alone and concomitantly with ketoconazole 400 mg once daily (QD); single dose before and single dose after rifampin 600 mg QD; Q12H where midazolam 7.5 mg was administered as a single dose alone before voclosporin and with last the dose buy lanoxin of voclosporin; Q12H alone and concomitantly with verapamil 80 mg every 8 h; and Q12H with digoxin 0.25 mg QD. The noncompartmental pharmacokinetic parameters maximal concentration (Cmax ) and area under the concentration-time curve (AUC) were obtained, and geometric least squares mean ratios and 90% confidence intervals were evaluated.

lanoxin usual dosage 2015-12-21

The mean age was 73.6 +/- 10.8 years. 50.5% were women and 49.5% men. Women (76.5 +/- 9.7 years) were older than men (70.5 +/- 11.0 years). The etiology was valvular heart disease 30.8%, hypertensive heart disease 26.2%, ischemic heart disease 21.6%, idiopathic dilated cardiomyopathy 8.2% and alcoholic cardiomyopathy 5.6%. The more frequent precipitating factors were respiratory infection (37.3%) and arrhythmias (28.7%). No precipitating buy lanoxin factor was detected in 13.9%. 46.1% had systolic disfunction (erection fraction < 50%). 96.7% were treated with diuretics, 79.3% with ACE inhibitors and 51.9% with digoxin. 5.3% needed cardiac surgery. Mean length of stay was 5.64 days. In hospital mortality was 5.6%.

lanoxin renal dose 2015-12-05

Varenicline had no clinically relevant effect on the digoxin steady-state exposure, as evidenced by the 90% confidence intervals for the ratios of AUC(0-24) (87.5-108%) and C(min) (83.8-116%) wholly contained within 80-125%. Digoxin C(max) and T(max) remained unchanged in the presence of varenicline, consistent with no apparent alteration in digoxin bioavailability. A minimal 11.3% increase in digoxin renal clearance was noted during varenicline treatment while having no buy lanoxin impact on its systemic exposure. Results are supported by mechanistic evidence in Caco-2 cell monolayers that varenicline is neither a P-gp substrate nor an inhibitor of P-gp-mediated efflux of digoxin. Co-administration of varenicline and digoxin was well tolerated.

lanoxin overdose antidote 2016-03-22

Increase of peroxisome proliferator-activated receptor δ (PPARδ) expression by digoxin in the heart of diabetic rats has been documented. The present study investigated the mediation of PPARδ in lipid metabolism improved by digoxin in the heart of diabetic rats and in the hyperglycemia-treated cardiomyocytes using the primary cultured cardiomyocytes from neonatal rat. The lipid deposition within the heart section was assessed Imdur Pill Identifier in diabetic rats by oil red O staining. The fatty acid oxidation genes in cardiomyocytes were also examined. Inhibitor of calcium ions and siRNA-PPARδ were employed to investigate the potential mechanisms. After a 20-day digoxin treatment, the PPARδ expression was elevated in hearts of diabetic rats while the cardiac lipid deposition was reduced. In neonatal cardiomyocytes, digoxin also caused an increase in expressions of PPARδ and fatty acid oxidation genes. But both actions of digoxin were blocked by BAPTA-AM to chelate calcium ions and by siRNA-PPARδ in cardiomyocytes. The obtained results show that increase of PPARδ by digoxin is related to regulation of fatty acid oxidation genes in cardiac cells mediated by calcium-triggered signals.

lanoxin 150 mg 2015-06-29

Diffuse spread through brain parenchyma and the presence of hypoxic foci rimmed by neoplastic cells are two cardinal features of glioblastoma, and low oxygen is thought to drive movement of malignant gliomas in the core of the lesions. Transcription factors associated with epithelial-to-mesenchymal transition (EMT) have been linked to this invasion, and we found that hypoxia increased in vitro invasion up to Lopid Normal Dosage fourfold in glioblastoma neurosphere lines and induced the expression of ZEB1. Immunohistochemical assessment of 295 surgical specimens consisting of various types of pediatric and adult brain cancers showed that ZEB1 expression was significantly higher in infiltrative lesions than less invasive tumors such as pilocytic astrocytoma and ependymoma. ZEB1 protein was also present in human fetal periventricular stem and progenitor cells and ZEB1 inhibition impaired migration of in vitro propagated human neural stem cells. The induction of ZEB1 protein in hypoxic glioblastoma neurospheres could be partially blocked by the HIF1alpha inhibitor digoxin. Targeting ZEB1 blocked hypoxia-augmented invasion of glioblastoma cells in addition to slowing them in normoxia. These data support the role for ZEB1 in invasive and high-grade brain tumors and suggest its key role in promoting invasion in the hypoxic tumor core as well as in the periphery.

lanoxin drug medication 2016-10-31

To analyse the changes in epidemiology, outpatient and emergency department clinical care, and outcomes of patients treated for acute heart failure (AHF Salbutamol Ventolin Dosage ) in Spanish hospital emergency departments (HEDs) between 2007 and 2014.

lanoxin drug interactions 2017-04-29

High-risk patients, during anesthesia and after surgery present changes in pharmacokinetics (biotransformation reactions, renal clearance, drug interactions, etc.) modifying the usefulness of most drugs, cardiac inotropics included. Aggrenox Online Pharmacy This group of substances is formed by adrenergic agents, phospodiesterase inhibitors and digitalis compounds. Adrenergic agents are the catecholamines, adrenaline (A), noradrenaline (NA) and dopamine (D), plus dopaminergic agonists as dobutamine and pirbuterol. Phosphodiesterase inhibitors, as amrinone and milrinone, produce their inotropic action by preserving cyclic adenosine monophosphate (AMPc) from its intracellular catabolism. Recent studies on the utility of digitalis compounds demonstrated the valuable applicability of digoxin in chronic and acute heart failure. Another group of substances whose mechanism of action differs from that of the inotropics, offers future utility in high risk patients, they include: inhibitors of nitric oxide sintases, natriuretic atrial peptide inhibitors, Q-10 coenzyme, endothelin antagonists, and anti-tumoral necrosis factor.

lanoxin maintenance dose 2015-01-10

To describe a patient with pulmonary and portal hypertension and to review the Paracetamol Acetaminophen Overdose pathogenesis and management of this condition.

lanoxin generic 2016-11-27

Spironolactone and potassium canrenoate (aldosterone antagonist diuretics) are often used with digoxin in clinical practice. It has been well documented in the literature that spironolactone, potassium canrenoate, and their common metabolite canrenone cross-react with several digoxin immunoassays at concentrations expected after therapeutic usage of these drugs and falsely elevate or lower serum digoxin concentrations. Recently, Abbott Laboratories marketed a new Digoxin Coumadin 2 Mg III immunoassay for application on the AxSYM analyzer. We studied the potential interference of these compounds with this new digoxin assay. The Tina-quant assay was used as the reference method because spironolactone, potassium canrenoate, and canrenone do not interfere with serum digoxin measurement using this assay. Aliquots of drug-free serum were supplemented with therapeutic and above therapeutic concentrations of spironolactone, canrenone, and potassium canrenoate, and apparent digoxin concentrations were measured using the Digoxin III assay and Tina-quant assay. Significant apparent digoxin concentrations were observed when the Digoxin III digoxin assay was used, but no apparent digoxin levels was observed using the Tina-quant assay. When serum pools prepared from patients receiving digoxin were further supplemented with these compounds in concentrations expected in sera of patients receiving these medications, falsely elevated digoxin levels were observed using Digoxin III assay, but no statistically significant change was observed using the Tina-quant assay. We conclude that spironolactone, potassium canrenoate, and their common metabolite canrenone interfere with the serum digoxin measurements using the new Digoxin III assay.