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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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Digoxin was not associated with increased all-cause mortality, survival free of admission due to any cause, or admission due to cardiovascular causes, regardless of underlying heart failure.

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Chronic heart failure is a common condition with a poor prognosis, usually associated with poor exercise tolerance and debilitating symptoms despite optimal modern therapy. Standard therapy includes diuretics, digoxin, angiotensin-converting enzyme inhibitors (ACEIs) and beta-blockers. Despite this, many patients remain symptomatic, and interest is high as to whether the angiotensin receptor blockers (ARBs) would offer further advantage to a patient already receiving quadruple therapy. In addition, some patients are intolerant of ACEIs, and for this group the ARBs seem a logical choice. This article reviews the evidence for the use of ARBs as a class in heart failure concentrating on clinical recommendations and clinical needs and evidence rather than purely on statistical issues of significance in trials. The trials to date have demonstrated clearly similar hemodynamic effects to those seen with ACEIs and variety of ancillary benefits such as improvements in endothelial function, anti-thrombotic effects, and effects on neurohormonal inhibition. There is consistent evidence of a preservation of exercise tolerance when patients with heart failure are crossed over from stable ACEI therapy, and when added to ACEIs exercise tolerance appears to increase with ARBs. In terms of major outcomes, the two largest trials, Elite-II and Val-Heft, demonstrate that angiotensin receptor blockers probably have a clinical role in improving mortality and morbidity as an alternative to ACEIs in those patients unable to tolerate these agents, which remain, however, the first choice in unselected patients with heart failure. There is a worrying suggestion of a negative interaction when ARBs are added to beta-blockers, which is a reason for caution in using the ARBs, not a reason not to use beta-blockers.

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Formation of inclusion bodies is a major limiting factor for secretory production of an antidigoxin single-chain antibody (SCA) fragment from Bacillus subtilis. To address this problem, three new strains with enhanced production of molecular chaperones were constructed. WB600BHM constitutively produces the major intracellular molecular chaperones in an appropriate ratio without any heat shock treatment. This strain reduced the formation of insoluble SCA by 45% and increased the secretory production yield by 60%. The second strain, WB600B[pEPP], overproduces an extracytoplasmic molecular chaperone, PrsA. An increase in the total yield of SCA was observed. The third strain, WB600BHM[pEPP], coproduces both intracellular and extracytoplasmic molecular chaperones. This led to a further reduction in inclusion body formation and a 2.5-fold increase in the secretory production yield. SCA fragments secreted by this strain were biologically active and showed affinity to digoxin comparable to the affinity of those secreted by strains without overproduction of molecular chaperones. Interestingly, accumulation of a pool of periplasmic SCA was observed in the PrsA-overproducing strains. This pool is suggested to represent the secreted folding intermediates in the process of achieving their final configuration.

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Subjects included all inpatients (n = 462) and outpatients (n = 437) receiving digoxin oral maintenance therapy for heart failure and/or atrial fibrillation with tachycardia at Kosei Hospital, Anjo, Japan. SDC and blood chemistry analysis were determined, and a 24-hour Holter electrocardiographic recording was performed when the SDC was at the presumed steady-state concentration.

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To evaluate the incremental differences of concurrent and persistent use of angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, loop diuretics, and digoxin on the one-year, all-cause risk of hospitalization and total healthcare costs associated with treatment of HF in patients enrolled in a managed care organization within the US.

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Transesophageal atrial pacing using the constant-rate technique was performed in 26 patients presenting with spontaneous atrial flutter (atrial cycle length between 180 and 270 ms). All but one patient had been treated with one or more antiarrhythmic agents (digoxin, quinidine, procainamide, propranolol, verapamil, diltiazem, and propafenone) within the previous 12 hours. Transesophageal atrial pacing at cycle lengths between 80 and 180 ms was successful in terminating atrial flutter in 22 patients: immediate reversion to sinus rhythm in 16, following transient sinus pause in one, following a brief period of atrial fibrillation in three, and following longer periods of atrial fibrillation in another two. No post-conversion ventricular arrhythmia and no other complications were observed. All patients experienced only a mild burning discomfort during the procedure. It is concluded that atrial pacing via the esophagus is a safe and noninvasive technique of terminating spontaneous atrial flutter. The effectiveness of this technique is comparable to endocardial or epicardial atrial pacing.

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Atrial fibrillation is the cardiac arrhythmia encountered most often in clinical practice. It is triggered by many conditions such as thyroid dysfunction, cardiac disease, alcohol, and pulmonary disease. Patients with chronic obstructive pulmonary disease (COPD) are susceptible to many insults that can lead to an acute deterioration superimposed on chronic disease. Changes in blood gases, abnormalities in pulmonary functions, and hemodynamic changes resulting from pulmonary hypertension can lead to the development of atrial fibrillation. Atrial fibrillation and COPD frequently coexist and complicate treatment of both conditions. The treatment of COPD exacerbation may include beta-adrenergic agonist and theophylline, which can precipitate atrial fibrillation with rapid ventricular response. Pharmacologic and electrical cardioversion may be ineffective in the management of atrial fibrillation in patients with COPD until respiratory decompensation has been corrected. This article focuses on the management of atrial fibrillation in patients with COPD.

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Twenty-two patients with severe congestive heart failure (New York Heart Association functional class III or IV with left ventricular ejection fraction of 18 +/- 1%) and 29 healthy male volunteers participated in this study. By combining direct sampling of internal jugular venous blood via a percutaneously placed catheter with a norepinephrine and epinephrine isotope dilution method for examining neuronal transmitter release, we were able to quantify the release of central nervous system monoamine and indoleamine neurotransmitters and investigate their association with the increased efferent sympathetic outflow that is variably present in treated patients with this condition. Mean cardiac norepinephrine spillover was 145% higher in treated heart failure patients than in healthy subjects (P < .05), with norepinephrine release from the heart in 6 of 22 patients being more than the highest control value. Raised internal jugular venous spillover of epinephrine (26 +/- 12 versus 2 +/- 4 pmol/min, P < .05) and of norepinephrine and its metabolites (2740 +/- 480 versus 875 +/- 338 pmol/min, P < .05), indicative of increased central nervous system turnover of both catecholamines, occurred in cardiac failure and was quantitatively linked to the degree of activation of the cardiac sympathetic nervous outflow, as was the jugular overflow of the principal serotonin metabolite, 5-hydroxyindoleacetic acid.

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Ezetimibe is the first lipid-lowering drug that inhibits intestinal uptake of dietary and biliary cholesterol without affecting the absorption of fat-soluble nutrients. Following oral administration, ezetimibe is rapidly absorbed and extensively metabolised (>80%) to the pharmacologically active ezetimibe-glucuronide. Total ezetimibe (sum of 'parent' ezetimibe plus ezetimibe-glucuronide) concentrations reach a maximum 1-2 hours post-administration, followed by enterohepatic recycling and slow elimination. The estimated terminal half-life of ezetimibe and ezetimibe-glucuronide is approximately 22 hours. Consistent with the elimination half-life of ezetimibe, an approximate 2-fold accumulation is observed upon repeated once-daily administration. The recommended dose of ezetimibe 10 mg/day can be administered in the morning or evening without regard to food. There are no clinically significant effects of age, sex or race on ezetimibe pharmacokinetics and no dosage adjustment is necessary in patients with mild hepatic impairment or mild-to-severe renal insufficiency. The major metabolic pathway for ezetimibe consists of glucuronidation of the 4-hydroxyphenyl group by uridine 5'-diphosphate-glucuronosyltransferase isoenzymes to form ezetimibe-glucuronide in the intestine and liver. Approximately 78% of the dose is excreted in the faeces predominantly as ezetimibe, with the balance found in the urine mainly as ezetimibe-glucuronide. Overall, ezetimibe has a favourable drug-drug interaction profile, as evidenced by the lack of clinically relevant interactions between ezetimibe and a variety of drugs commonly used in patients with hypercholesterolaemia. Ezetimibe does not have significant effects on plasma levels of HMG-CoA reductase inhibitors commonly known as statins (atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin), fibric acid derivatives (gemfibrozil, fenofibrate), digoxin, glipizide, warfarin and triphasic oral contraceptives (ethinylestradiol and levonorgestrel). Concomitant administration of food, antacids, cimetidine or statins had no significant effect on ezetimibe bioavailability. Although coadministration with gemfibrozil and fenofibrate increased the bioavailability of ezetimibe, the clinical significance is thought to be minor considering the relatively flat dose-response curve of ezetimibe and the lack of dose-related increase in adverse events. In contrast, coadministration with the bile acid binding agent colestyramine significantly decreased ezetimibe oral bioavailability (based on area under the plasma concentration-time curve of total ezetimibe). Hence, ezetimibe and colestyramine should be administered several hours apart to avoid attenuating the efficacy of ezetimibe. Finally, higher ezetimibe exposures were observed in patients receiving concomitant ciclosporin, and ezetimibe caused a small but statistically significant effect on plasma levels of ciclosporin. Because treatment experience in patients receiving ciclosporin is limited, physicians are advised to exercise caution when initiating ezetimibe in the setting of ciclosporin coadministration, and to carefully monitor ciclosporin levels.

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The low therapeutic index of digoxin necessitates careful monitoring of its serum levels. Most of digoxin immunoassays suffer from interferences with digoxin-like immunoreactive substances. Since aptamers have been shown to be highly specific for their targets, the aim of this study was to develop DNA aptamers for this widely used cardiac glycoside. Digoxin was coated onto the surface of streptavidin magnetic beads. DNA aptamers against digoxin were designed using Systematic Evolution of Ligands by Exponential enrichment method (SELEX) by 11 iterative rounds of incubation of digoxin-coated streptavidin magnetic beads with synthetic DNA library, DNA elution, electrophoresis and PCR amplification. The PCR product was cloned and sequenced. Binding affinity was determined using digoxin-BSA conjugate, coated onto ELISA plate. Inhibitory effect of anti-digoxin aptamer was conducted using isolated guinea-pig atrium. Three aptamers (D1, D2 and D3) were identified. Binding studies of fluorescein-labeled truncated (without primer binding region) D1 and D2 and full length D1 anti-digoxin aptamers were performed and their corresponding dissociation constants values were 8.2×10(-9), 44.0×10(-9) and 17.8×10(-9) M, respectively. This is comparable to what other workers have obtained for interaction of monoclonal antibodies raised against digoxin. There was little difference in binding affinity between full length and truncated anti-digoxin D1 aptamer. D1 anti-digoxin aptamer also inhibited the effects of digoxin on the isolated guinea-pig atrium. D1 anti-digoxin aptamer distinguished between digoxin and ouabain in both tissue study and binding experiments. Our finding indicated that D1 anti-digoxin aptamer can selectively bind to digoxin. Further studies might show its suitability for use in digoxin assays and as a therapeutic agent in life-threatening digoxin toxicity.

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In the total population [n = 2,739, with 97 (3.5%) Hispanics, 66.6 +/- 11.6 years, 70.9% male, 66.9% valve surgery], Hispanics were 38% less likely to develop AF (15.5% vs 24.8%, P = 0.035). However, the Hispanic patients were 11.9 years younger (P< 0.001) with 14.7% more women (P = 0.002) which reduces the risk of post-CTS AF; they also had a 12.8% higher risk of valvular surgery (P = 0.009) which is known to enhance the risk. When these factors and other important variables were matched for, a total of 485 patients (n = 97 Hispanics, 388 Caucasian) were evaluated (55.8 +/- 13.1 years, 57.3% male, 45.4% valvular surgery). Hispanic and Caucasian patients had a similar incidence of post-CTS AF (15.5% vs 18.3%, P = 0.513).

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Although ventricular cardiomyocytes express inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] receptors, it is unclear how these Ca2+ channels contribute to the effects of Gq-coupled agonists. Endothelin-1 augmented the amplitude of pacing-evoked Ca2+ signals (positive inotropy), and caused an increasing frequency of spontaneous diastolic Ca2+-release transients. Both effects of endothelin-1 were blocked by an antagonist of phospholipase C, suggesting that Ins(1,4,5)P3 and/or diacylglycerol production was necessary. The endothelin-1-mediated spontaneous Ca2+ transients were abolished by application of 2-aminoethoxydiphenyl borate (2-APB), an antagonist of Ins(1,4,5)P3 receptors. Incubation of electrically-paced ventricular myocytes with a membrane-permeant Ins(1,4,5)P3 ester provoked the occurrence of spontaneous diastolic Ca2+ transients with the same characteristics and sensitivity to 2-APB as the events stimulated by endothelin-1. In addition to evoking spontaneous Ca2+ transients, stimulation of ventricular myocytes with the Ins(1,4,5)P3 ester caused a positive inotropic effect. The effects of endothelin-1 were compared with two other stimuli, isoproterenol and digoxin, which are known to induce inotropy and spontaneous Ca2+ transients by overloading intracellular Ca2+ stores. The events evoked by isoproterenol and digoxin were dissimilar from those triggered by endothelin-1 in several ways. We propose that Ins(1,4,5)P3 receptors support the development of both inotropy and spontaneous pro-arrhythmic Ca2+ signals in ventricular myocytes stimulated with a Gq-coupled agonist.

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A retrospective analysis of data collected prospectively on 400 consecutive valve surgery patients between May 2002 and December 2012 was performed. Patients were grouped according to avoidance or insertion of temporary pacing wires, and were further subdivided according to temporary cardiac pacing need. Multiple logistic regression was used to determine the predictors of temporary cardiac pacing.

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In vitro and clinical studies were conducted to characterize the potential of avasimibe, an acyl-CoA/cholesterol acyltransferase inhibitor to cause drug-drug interactions. Clinically, 3- and 6-fold increases in midazolam (CYP3A4 substrate) oral clearance were observed after 50 and 750 mg of avasimibe daily for 7 days, respectively. A 40% decrease in digoxin (P-glycoprotein substrate) area under the curve was observed with 750 mg of avasimibe daily for 10 days. In vitro studies were conducted to define the mechanisms of these interactions. Induction was observed in CYP3A4 activity and immunoreactive protein (EC50 of 200-400 nM) in primary human hepatocytes treated with avasimibe. Rifampin treatment yielded similar results. Microarray analysis revealed avasimibe (1 microM) increased CYP3A4 mRNA 20-fold, compared with a 23-fold increase with 50 microM rifampin. Avasimibe induced P-glycoprotein mRNA by about 2-fold and immunoreactive protein in a dose-dependent manner. Transient transfection assays showed that avasimibe is a potent activator of the human pregnane X receptor (hPXR) and more active than rifampin on an equimolar basis. Drug-drug interaction studies for CYP3A4 using pooled human hepatic microsomes and avasimibe at various concentrations, revealed IC50 values of 20.7, 1.6, and 3.1 microM using testosterone, midazolam, and felodipine as probe substrates, respectively. Our results indicate that avasimibe causes clinically significant drug-drug interactions through direct activation of hPXR and the subsequent induction of its target genes CYP3A4 and multiple drug resistance protein 1.

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The purpose of this study was to ascertain the presence of gender bias in the medical management of heart failure, and to assess its association with the specialty of the caregiver physician.

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The ability to stimulate cardiac contractility is known as positive inotropy. Endogenous hormones, such as adrenaline and several natural or synthetic compounds possess this biological property, which is invaluable in the modern cardiovascular therapy setting, especially in acute heart failure or in cardiogenic shock. A number of proteins inside the cardiac myocyte participate in the molecular pathways that translate the initial stimulus, that is, the hormone or drug, into the effect of increased contractility (positive inotropy). Genetic variations (polymorphisms) in several genes encoding these proteins have been identified and characterized in humans with potentially significant consequences on cardiac inotropic function. The present review discusses these polymorphisms and their effects on cardiac inotropy, along with the individual pharmacogenomics of the most important positive inotropic agents in clinical use today. Important areas for future investigations in the field are also highlighted.

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Anchored periplasmic expression (APEx) is a method for isolating high affinity ligand-binding proteins from large combinatorial libraries, and antibodies highly specific for soluble antigens were successfully isolated from APEx antibody libraries in combination with flow cytometric sorting (Harvey et al., Proc Natl Acad Sci USA 101(25):9193-9198, 2004). However, many disease markers and drug targets are localized on the cell surface, and often, unique posttranslational modifications and/or properly folded epitopes are lost when they were expressed and isolated in soluble form. In this study, we demonstrate that Escherichia coli spheroplasts, displaying antibodies and screened by a combination of plate-panning and flow cytometric sorting, can be used for isolating antibodies specific for antigens on the human cell surface. Two rounds of plate-panning followed by one round of flow cytometric sorting resulted in 7,200-fold enrichment of antibodies specific for the protective antigen of Bacillus anthracis from a large excess of spheroplasts expressing a scFv antibody to digoxin (a negative control). There is the potential to use this technique for library screening to find novel antibodies against disease cell surface antigens.

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To identify risk factors, patient characteristics, and medications associated with a higher likelihood of ADEs in adult inpatients through an overview of reviews on this topic.

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These results indicate that OATP1B1 and OATP1B3 are at least partly responsible for the accumulation of TR-14035 into hepatocytes, and Mrp2 principally mediates the biliary excretion of TR-14035. Furthermore, genetic polymorphisms of OATP1B1 may cause an interindividual variability in the pharmacokinetics of TR-14035.

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Sixty-seven adults (32 men, 35 women) with chronic heart failure or atrial fibrillation who were receiving digoxin therapy.

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The contractile behavior of cardiomyocytes can be monitored by measuring their action potentials, and the analysis is essential for screening the safety of potential drugs. However, immobilizing cardiac cells on a specific electrode is considerably complicated. In this study, we demonstrate that scanning electrochemical microscopy (SECM) can be used to analyze rapid topographic changes in beating cardiomyocytes in a standard culture dish. Various cardiomyocyte contraction parameters and oxygen consumption based on cell respiration could be determined from SECM data. We also confirmed that cellular changes induced by adding the cardiotonic agent digoxin were conveniently monitored by this SECM system. These results show that SECM can be a potentially powerful tool for use in drug development for cardiovascular diseases.

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Chronic heart failure (CHF) is common, disabling and deadly. Recent studies show that ACE inhibitors reduce morbidity and mortality in all grades of CHF and may even delay or prevent the onset of overt CHF in patients with asymptomatic left ventricular dysfunction. In this review, guidelines are given for how to use these drugs both in hospital and in general practice. New evidence on the benefits of digoxin is also considered, and the management of concomitant problems such as angina and arrhythmias in patients with CHF is discussed.

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The two agents beta-methyldigoxin (medixin), a Soviet medilazide, and bemecor (digicor), a foreign analogue (LEK, Yugoslavia) were comparatively evaluated. An equal high (85%) clinical efficacy of the drugs was found in 81 patients with varying stages of heart failure. A positive therapeutic effect was accompanied by lower heart rate, higher diuresis and natri-and kaliuresis, decreased systolic and diastolic pressures in the pulmonary artery. The incidence of adverse reactions and the causes of their occurrence are analyzed.

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To investigate the interaction of cardiac glycosides with vasoconstrictors, we examined the effects of short term treatment with the cardiac glycoside digoxin (6 mg/kg/day, i.p., for 6 days) in rats made hypertensive by chronic infusion of norepinephrine (NE), angiotensin II (A II) or vasopressin (VP). When digoxin was administered simultaneously with NE at 1.8 mg/kg/day (i.p.) by use of osmotic minipumps in conscious rats, systolic blood pressure decreased to 120 +/- 3 mmHg on Day 1 whereas it rose to 148 +/- 2 mmHg in rats given NE alone (p less than 0.01). The antihypertensive effect of digoxin was sustained for the entire experimental period and was not associated with any change in urinary sodium excretion. When the same dose of digoxin was administered simultaneously with A II at 900 micrograms/kg/day (i.p.) in conscious rats, systolic blood pressure rose to a greater extent than in those given A II alone. The administration of digoxin had no effect on the blood pressure elevation induced by chronic infusion of VP at a rate of 7.2 U/kg/day (i.p.). It is concluded that short term treatment with digoxin has a variety of effects on blood pressure in rats; pressor, depressor, or is no effects depending upon vasoconstrictor used.

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Elevated levels of endogenous digoxin-like immunoreactivity have been reported in the body fluids of premature and full-term infants as well as in term pregnancy, in the amniotic fluid, and in human milk. Several lines of evidence suggest that these factors could also have biological properties in common with digitalis: i.e., they could represent truly endogenous digitalis-like factor(s). In recent years we succeeded in partially purifying this factor from umbilical cord blood, which represents an easily available source of this factor. The inhibitory activity of this factor on 86Rb uptake could be neutralized by antidigoxin antibodies (Fab fragments) and provided, for the first time, direct evidence of an association between digoxin-like immunoreactivity and biological digitalis-like activity. In addition, these antibodies could be used for immunoaffine chromatography as a purification step before separation by high-performance liquid chromatography. Preliminary experiments suggest that this endogenous compound has both a tissue and an isoenzyme selectivity and is not a well-known steroid (testosterone, progesterone, 17-OH progesterone, cortisol, dehydroepiandrosterone sulfate, and estradiol).

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lanoxin overdose death 2016-09-08

Patients were admitted and given oral sotalol in an inpatient, monitored setting. buy lanoxin The initial dose was targeted at 2 mg/kg. Antiarrhythmic drugs other than digoxin were stopped.

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P-glycoprotein (P-gp) and organic anion transporting polypeptides (Oatp) are expressed at the blood-brain barrier (BBB). There is little functional evidence for Oatp-mediated transport at the BBB. The peptidic delta opioid-receptor agonist [D-penicillamine(2,5)]-enkephalin (DPDPE) is a substrate of mdr1a P-gp and Oatp2. The present study evaluated the influence of these transporters on brain uptake of DPDPE by in situ perfusion in mice. Brain uptake was increased approximately buy lanoxin 12-fold in mice lacking P-gp in the BBB, but the P-gp inhibitor dexverapamil did not increase uptake in P-gp-competent mice. In P-gp-deficient mice, DPDPE uptake was saturable (K(m) approximately 24 mM), and was inhibited by dexverapamil and the Oatp2 substrates digoxin, estradiol-17beta-glucuronide and fexofenadine. These results confirm P-gp-mediated efflux of DPDPE, and suggest functional uptake transport of DPDPE by Oatp, at the murine BBB.

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A MEDLINE search was conducted. Scientific studies, case report and review articles were collected buy lanoxin . Papers published demonstrating drugs interfering with MIBG uptake were evaluated.

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Controversy continues concerning the clinical utility of digoxin in women with HF. buy lanoxin

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Neonatal atrial flutter is an arrhythmia with significant acute morbidity but an excellent long-term prognosis. Electrical cardioversion is the first-choice treatment when the arrhythmia is not well-tolerated hemodynamically, while class III buy lanoxin antiarrhythmic drugs such as amiodarone should be preferred in the other cases.

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There were three parts to the study: digoxin once daily plus placebo three times daily for 1 week; digoxin once daily plus ropinirole three times daily for 6 weeks; and digoxin once daily plus placebo three times daily for 1 week. Serial blood samples were collected over 24 h at the end of each part of the study for buy lanoxin pharmacokinetic assessment. Pre-dose blood samples were collected on specific days throughout the study to assess the attainment of steady-state plasma levels of digoxin. The primary endpoints were AUC(0, tau) and Cmax for digoxin.

lanoxin tab 2015-06-12

Each of 5 drugs, i.e., 4 different vasodilator drugs (captopril, enalapril, hydralazine and prazosin) and a cardiotonic drug (digoxin), was administered to dogs with mitral regurgitation (MR) for 1-72 days in order to quantitatively evaluate the influence of therapeutic agents on blood flow in heart disease. Hemodynamic changes were assessed before and after administration of each drug by determining mitral regurgitant jet mapping area (MRMA) and aortic forward flow mapping area (AFMA), which were displayed by the color Doppler method, and the ratio of MRMA to AFMA (MRMA/AFMA) as parameters. When the four vasodilator drugs were used appropriately, MRMA and MRMA/AFMA decreased in all cases, compared with the values before the administration. These two parameters showed dose-dependent changes after administration of captopril, enalapril and hydralazine. When the cardiotonic drug was used. MRMA and MRMA/AFMA increased in 4 of 5 cases. The MRMA/AFMA values were slightly more reproducible than the MRMA values, whereas the AFMA values showed buy lanoxin no constant tendency when any vasodilator drug or the cardiotonic drug was used. These results suggest that the efficacy of cardiotonic and vasodilator drugs in MR can be quantitatively evaluated by determining MRMA/AFMA in particular, and MRMA.

lanoxin 150 mg 2015-08-27

In order to specify that protein labeling is the result of mono-ADP ribosylation, a careful evaluation of the reaction conditions and products is necessary. To investigate the specificity and target proteins of the arginine-specific mono-ADP-ribosyltransferase (mADP-RT) in rabbit skeletal muscle buy lanoxin T-tubules (TT) biotin- or digoxigenin-coupled NAD-derivatives were synthesized. They were used for the nonradioactive labeling of proteins and compared with radioactive mono-ADP-ribosylation. According to the results of our studies, they cannot be used as substrates to detect arginine-specific or pertussis toxin-dependent mono-ADP-ribosylation of target proteins in skeletal muscle. In contrast, radioactive NAD can be used to monitor these reactions. Under the appropriate reaction conditions, the radioactive [adenylate-14C]NAD and [32P]NAD were found to be solely consumed by the arginine-specific mADP-RT of skeletal muscle TT. The incorporation studies confirmed earlier data on the localization of the mADP-RT and its targets in TT. The T-tubular targets were purified in a single-step procedure using phenylboronate affinity chromatography. Of 18 target proteins delineated by autoradiography of electrophoretically separated T-tubular proteins, a 42-kDa protein was suggested to be the stimulatory G protein (Gsalpha). Mono-ADP-ribosylation of Gsalpha resulted in an inhibition of the T-tubular adenylate cyclase activity as proven by the suppression of this inhibition using novobiocin as a specific inhibitor of mADP-RT.

lanoxin 250 mg 2017-01-21

ReMeFa was a multicenter, prospective, descriptive study. We included adults with documented AF. We excluded those with AF secondary to reversible causes, undergoing pulmonary vein ablation, pacemaker or defibrillator users, with a life expectancy of less than one year, or with physical or mental impediments to meet the protocol objectives. Data were collected at baseline and at 6 buy lanoxin and 12 months.

lanoxin 500 mg 2016-06-08

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic buy lanoxin blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)

lanoxin 2 mg 2015-02-16

Using 100 microl of plasma sample, the lower limit of quantitation for antipyrine (10 pg/ml), carbamazepine (1 pg/ml), metoprolol (5 pg/ml), atenolol (20 pg/ml), and digoxin (5 pg/ml) were achieved using an API 5000. Proportional pharmacokinetics were observed from 0.167 microg/kg to 1 buy lanoxin ,670 microg/kg for antipyrine and carbamazepine and from 1.67 to 1,670 microg/kg for atenolol and digoxin, while metoprolol exhibited a non-proportional pharmacokinetics relationship. Several metabolites of carbamazepine were characterized in plasma from rats dosed at 1.67 mug/kg using LC-MS/MS.

lanoxin 60 mg 2015-02-27

The present study experimentally demonstrated for the first time the presence of pre-miRNA and miRNA buy lanoxin in the human mitochondria isolated from skeletal muscular cells. A set of miRNA were significantly detected in mitochondria fraction. The origin of these pre-miRNA and miRNA should be further investigate to determine if they are imported from the cytosol and/or if they are partially processed in the mitochondria.

lanoxin pill identifier 2016-05-08

Non-radioactive digoxigenin (DIG)-labelled probes that can differentiate porcine circovirus (PCV) 1 from PCV2 in formalin-fixed, paraffin-wax-embedded tissues by in-situ hybridisation were developed. A 349 base pair (bp) DNA fragment from open reading frame (ORF) 1 of PCV1 and a 481 bp DNA fragment from ORF2 of PCV2 generated by polymerase chain reaction (PCR) were used as PCV1 and PCV2 probes, respectively. A specific DIG-labelled PCV1 DNA probe did not hybridise with PCV2-infected PK-15 cells buy lanoxin and vice versa. From the 40 field cases with postweaning multisystemic wasting syndrome tested by in-situ hybridisation, 30 (75 per cent) cases were PCV2-positive only and 10 (25 per cent) cases were positive for both PCV1 and PCV2. PCV1 and PCV2 DNAS were detected mainly in the macrophages of lymph nodes and spleens. Positive cells typically exhibited a dark brown to black reaction product mainly in the cytoplasm but also occasionally in the nucleus. In-situ hybridisation together with the differential probes developed in the present study represent an additional tool capable of differentiating of both types of PCV in formalin-fixed, paraffin-wax-embedded tissues.

lanoxin 125 mg 2015-04-29

In situ hybridization experiments, using oligodeoxyribonucleotides specific for the two major expressed human tyrosine hydroxylase mRNAs, were performed on human brain sections at the level of the mesencephalon. The specificity of the probes was ascertained by Northern blot experiments carried out with independently in vitro synthesized human tyrosine hydroxylase mRNAs. For in situ hybridization experiments, oligodeoxyribonucleotides were labelled with nucleotides tagged with digoxigenin or biotin molecules. The hybridized oligonucleotides were detected by antibodies coupled with peroxidase and alkaline phosphatase enzymes, which yield, with appropriate substrates, brown and purple products, respectively. The simultaneous detection of the two mRNAs with digoxigeninated and biotinylated probes revealed that these two mRNAs are co-expressed in single cells. The purple product obtained with alkaline phosphatase exhibits a discrete distribution within the dopaminergic cells suggesting these mRNAs are associated with sub-cellular structures. Finally, a heterogeneity in the intensity of the labelling of reactive cells with both buy lanoxin probes was visualized as well as the expression of the two mRNA species in neurites.

lanoxin and alcohol 2017-10-02

After randomly assigned pretreatment with either verapamil or digoxin Risperdal Generic Name for four weeks, DC cardioversion was performed. If sinus rhythm was restored then verapamil treatment was discontinued.

lanoxin yellow tablet 2016-03-11

To undertake a pilot study before conducting a Cymbalta Good Reviews large European multicentre prospective study, to determine the proportion of patients with atrial fibrillation who were not receiving antithrombotic treatment before stroke onset, and their characteristics.

lanoxin overdose symptoms 2017-11-04

We used computerized alerts to identify patients Plavix 150mg Dose with laboratory values that could be related to medication errors associated with digoxin and warfarin. Over a six-week period at two inpatient facilities, we generated 62 laboratory-based alerts for warfarin, and 66 for digoxin. The positive predictive value for these alerts representing a preventable event was 71% and 57% for warfarin and digoxin, respectively.

lanoxin generic substitution 2015-12-16

As part of a larger clinical drug-drug interaction (DDI) study aimed at in vitro to in vivo prediction of HIV protease inhibitor metabolic and transporter-based DDIs, we measured the inductive (staggered administration) and inductive plus inhibitory (simultaneously administered) effect of multiple dose ritonavir (RTV), nelfinavir (NFV), or rifampin (RIF) on the pharmacokinetics of the P-glycoprotein probe, digoxin (DIG), when administered simultaneously or staggered with the protease inhibitors or RIF. In both cases, NFV did not significantly affect DIG disposition. RTV decreased DIG renal clearance Glucophage Drug Label (Cl(renal)) when administered simultaneously or staggered but significantly increased DIG area under the curve from time zero to 24 h (AUC(0-24 h)) only when administered simultaneously. RIF decreased DIG AUC(0-24 h) only when RIF and DIG administration was staggered. When RIF and DIG were administered simultaneously, DIG maximal observed plasma concentration and area under the curve from time zero to 4 h were significantly increased, and DIG Cl(renal) was decreased. An unexpected and potentially clinically significant DDI was observed between DIG and the CYP2B6 probe, bupropion, which decreased DIG AUC(0-24 h) 1.6-fold and increased Cl(renal) 1.8-fold. Because this was an unexpected DDI and our studies were not specifically designed to quantify this interaction, further studies are required to confirm the interaction and understand the mechanistic basis of the DDI. In summary, RTV or NFV do not induce P-glycoprotein activity measured with DIG, and RIF does so only under staggered administration.

lanoxin prices 2017-05-12

Ouabain has been reported to increase the secretion of ANP in vitro. In this study, we focused on whether this action is common in Na-K-ATPase inhibitors (ATPI) and whether ATPI simply increase the release of ANP or stimulate both its biosynthesis and release. The effects of ouabain and digoxin on secretion of ANP and accumulation of ANP mRNA were investigated in the rat cardiocyte superfusion system. Ouabain and Lasix 600 Mg digoxin increased the immunoreactive ANP (iANP) output into perfusate and accumulation of ANP mRNA significantly. These results suggest that ATPI may stimulate both ANP biosynthesis and release in vitro.

lanoxin 25 mg 2017-10-14

The odds ratio (OR) of treated group compared with control was estimated for each end-point outcome and plotted against each other using the fixed-effects model Imodium Drug Use . THE MAIN OUTCOME MEASURES: The primary outcomes of our analysis were effects of diuretics on mortality and morbidity.

lanoxin drug guide 2015-12-03

TDM service is much less than optimal in SQUH. A lot of effort Flagyl Generic needs to be carried out to improve TDM use in the developing countries as adjusting the doses on results that are based on wrong sampling time might expose patients to toxicity or therapeutic failure.

lanoxin overdose effects 2015-10-04

Patients in I-PRESERVE are broadly representative of those seen in epidemiological studies and, because of this, the results of this trial should be generally applicable to Stromectol Brand Name "real world" patients with heart failure and preserved ejection fraction.

lanoxin drug study 2017-10-14

Omeprazole, a proton pump inhibitor (PPI), is widely used for the treatment of dyspepsia, peptic ulcer, gastroesophageal reflux disease, and functional dyspepsia. Polypharmacy is common in patients receiving omeprazole. Drug toxicity and treatment failure resulting from inappropriate combination therapy with omeprazole have been reported sporadically. Systematic review has not been available to address the pharmacokinetic drug-drug interaction (DDI) profile of omeprazole with adverse consequences, the factors determining the degree of DDI between omeprazole and comedication, and the corresponding clinical risk management. Aldactone 150 Mg

lanoxin overdose 2017-09-05

An improved chemiluminescence-based RNA/DNA detection procedure offering a widely applicable alternative to the conventional 32P labeling employed in molecular biology is described. Even highly sensitive applications such as Northern blot analysis of low-copy RNAs are shown to be feasible now without radioactive labeling. Improved quality of nonradioactive detection was obtained by the use of digoxigenin-labeled nucleotides in combination with dioxetane substrates which are decomposed by the hydrolysis of alkaline phosphatase. Previously existing problems involving unacceptably high background signals in nonradioactive labeling procedures were eliminated by the application of a modified RNA/DNA transfer, hybridization, and detection protocol. The data presented here delineate a system consistently superior to radioactivity and should considerably increase the usefulness of nonradioactively labeled probes detected by chemiluminescence.

lanoxin tablets dosage 2015-08-25

We describe the cloning, functional characterization and tissue localization of a novel membrane transporter of the OATP/Oatp-gene family obtained from liver and kidney of cattle (Bos taurus). The carrier protein exhibits highest sequence identity to the human OATP1A2 (previously called OATP-A) and is, therefore, named bovine Oatp1a2. Bovine Oatp1a2 received the gene symbol Slco1a2 that is identical to the SLC classification of human OATP1A2 (SLCO1A2, previously called SLC21A3) and is likely an orthologue of the human gene. Two different full-length bOatp1a2 cDNAs of 2316-bp and 3504-bp were obtained and encoded for a 666 amino acid membrane protein, which contains twelve putative transmembrane spanning domains. Bovine Oatp1a2 expression was detected in liver, kidney, brain and adrenal gland. Uptake studies in cRNA-injected oocytes demonstrated that bOatp1a2 transports estrone-3-sulfate and taurocholate, with K(m) values of 9.6 microM and 51 microM, respectively, and estradiol-17beta-glucuronide. However, the structurally-related heart glycosides ouabain (1 microM) and digoxin (1 microM) are neither transported by bovine Oatp1a2 nor by human OATP1A2. We conclude that based on the tested substrates bovine Oatp1a2 shows functional homology to human OATP1A2.