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Lasix (Furosemide)

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Lasix is a highly effective FDA approved medication for the treatment of excessive edema (fluid retention) due to kidney disorder (nephrotic syndrome), heart failure, cirrhosis and liver disease. It is also used to treat high blood pressure (hypertension). Lasix works by regulating the way in which the body absorbs salts.

Other names for this medication:
Aldalix, Anfuramide, Ansemid, Apix, Apo-furosemida, Asax, Betasemid, Diaqua-2, Foliront, Salix®, Frusenex, Frusemide, Furantral, Furesis, Furetic, Furide, Furocot, Furovet, Furoxem, Furozenol, Fursemid, Furtenk, Fusix, Hoe 058, Inclens, Intermed, Jufurix, Las 6873, Lasilacton, Lasilactone, Lasiletten, Lasilix, Lo-Aqua, Vesix

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Also known as:  Furosemide.


Lasix prevents excessive edema (fluid retention) in people with kidney disorder (nephrotic syndrome), heart failure, cirrhosis and liver disease. It is also used for the treatment of high blood pressure (hypertension), high levels of potassium (hyperkalemia), calcium (hypercalcemia), and magnesium (hypermagnesemia).

The active component, Furosemide, is a potent loop diuretic (water pill) that eliminates water and salt from the body. Furosemide works by blocking the absorption of sodium, chloride, and water from the filtered fluid in the kidney tubules, causing a profound increase in the output of urine (diuresis).

Lasix starts to act within one hour after oral administration, and the effect lasts for about 6-8 hours.


Lasix is available in tablets which should be taken orally with a full glass of water.

The dosage of Lasix depends on the body weight and on the health status of the recipient.

Take Lasix at the same time once a day.

Do not take more than your recommended dose, as high doses of furosemide may cause irreversible hearing loss.

Do not crush or chew the tablet.

To achieve the most effective results, do not stop taking Lasix suddenly.


In case of a Lasix overdose visit your doctor or health care provider immediately. Symptoms of a Lasix overdose include fainting, tinnitus, confusion, weakness, lightheadedness, 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 Lasix 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 Lasix if you are allergic to any of its components or if you are unable to urinate.

Do not take Lasix if you are pregnant, plan to have a baby, or you are breastfeeding.

Do not take Lasix if you suffer from or have a history of kidney disease, cirrhosis or other liver disease, gout, lupus or diabetes.

Do not take Lasix if you suffer from enlarged prostate, bladder obstruction or other urination problems, or an electrolyte imbalance (such as low levels of potassium or magnesium in your blood).

Do not take Lasix if you suffer from high cholesterol or triglycerides (a type of fat in the blood).

Use Lasix with care if you are taking indomethacin (such as Indocin); steroids (such as prednisone); diabetes medicines; diet pills; sucralfate (such as Carafate); netilmicin (such as Netromycin); amikacin (such as Amikin); streptomycin; tobramycin (such as Nebcin, Tobi); gentamicin (such as Garamycin); digoxin (such as Lanoxin); blood pressure medicines; salicylates (such as aspirin, Tricosal, Disalcid, Dolobid, Salflex, Doan's Pills); cold medicines; lithium (such as Lithobid, Eskalith), ethacrynic acid (such as Edecrin); probenecid (such as Benemid).

This medicine can make your skin more sensitive to the sunlight. Try to protect your skin where possible.

Avoid becoming dehydrated.

If you are going to have surgery, inform your doctor that you are taking Lasix.

Do not stop taking Lasix suddenly.

lasix 40 mg

To investigate the relationship between the plasma ANP concentration and left ventricular end-diastolic pressure (LVEDP) in healthy calves subjected to volume overload (Study 1), and to compare the plasma ANP concentration in calves with or without heart disease (Study 2).

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There were 16 episodes of ARF in 14 patients and 62.5 % were male (mean 6 SD age: 50 +/- 49 months). The incidence of ARF was 2.5 % of PICU patients. The most frequent primary diseases were nephro-urological (50 %) and heart disease (31 %). The main risk factors for ARF were hypovolemia (44 %) and hypotension (37 %). Six patients (37.5 %) developed ARF following surgery (cardiac surgery in four, kidney transplantation in one and urological surgery in one). Furosemide was used in 13 patients (as continuous perfusion in nine), inotropes in nine and renal replacement therapy in 12. Medical complications were found in 94 % and some organic dysfunction was found in 81 %. The length of stay in the PICU was 21 +/- 21 days. The probability of death according to the Pediatric Risk of Mortality was 14 +/- 8 %. Five patients died (36 % of the patients and 31.2 % of ARF episodes).

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From February to June 1995, 7 patients with end-stage heart failure underwent partial left ventriculectomy. Before the surgical procedure, 7 (100%) patients were in functional class IV. Three (42%) patients needed inotropic support for hemodynamic stability. The mean daily dose of furosemide was l48.67 +/- 128.27 mg, of captopril 87.50 +/- 95.20 mg and of digoxin 0.23 +/- 0.04. Mean left ventricular diastolic dimension determined by 2-D echocardiography was 78.29 +/- 12.63 mm, mean left ventricular ejection fraction, determined by radionuclide ventriculography, was 0.15 +/- 0.05 whereas mean transpulmonary gradient and pulmonary vascular resistance in Wood units, determined by right heart catheterization, were 16.80 +/- 8.80 and 6.57 +/- 3.22, respectively.

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Nephrotoxicity of nonsteroidal anti-inflammatory drugs is associated with other risk factors (volume-depletion) and may be secondary to functional changes mediated by the inhibition of renal cyclooxygenases. Acute anti-inflammatory doses of flosulide and indomethacin were determined on carrageenan paw edema and its effects on renal plasma flow (RPF) and glomerular filtration rate (GFR) were studied in normovolemic and hypovolemic rats. In normovolemic rats, flosulide increased RPF and GFR (25 mg/kg) and indomethacin (5-10 mg/kg) was without effect. Volume-depleted rats were obtained by oral furosemide (32 mg/kg), urinary eicosanoids were determined. After furosemide, plasma volume, RPF and GFR and PGE2 decreased. Treatment of hypovolemic rats with flosulide (5-25 mg/kg) or indomethacin 10 mg/kg reduced RPF and GFR. Flosulide at 5 mg/kg reduced 6-keto-PGF1alpha whereas at 25 mg/kg and after indomethacin at 10 mg/kg a fall in 6-keto-PGF1alpha and TXB2 appeared. Our data suggest that acute COX-2 selective inhibition may alter renal function.

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An 80-year-old female was admitted to our emergency Coronary Unit presenting symptoms and signs of shock with acute pulmonary edema. Patient was hospitalised at the Opthalmological Department with intention to undergo cataract surgery. Approximately, four hours before operation, half a tablet of acetazolamide 250 mg was given, in order to control her pre-operative intraocular pressure. Half an hour later, she complained of nausea, became cyanotic, and suffered acute respiratory failure with characteristic massive pulmonary edema. Ventilatory support was initiated and O2 saturation increased to 89%. She was administered 2 ampoules of intravenously furosemide. The blood chemistry panel was normal, as well as myocardial cytolysis tests. Chest radiograph showed enlarged cardiothoracic index, ill-defined vessels, peribronchial cuffing, alveolar edema. An echocardiogram showed normal atria and ventricles, normal systolic function, and excluded pulmonary hypertension. Furosemide (40 mg/IV, S: 1x3) and oxygen (8 Lt/min) were administered for the following 24 hours. Clinical improvement was seen and the O2 saturation was normalized. ECG controls were normal. The patient experienced a full recovery and was discharged 3 days later.

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Overlap between urinary and tumor radioactivity was observed in 8 of 133 scans (6%) in patients who receive furosemide and in 3 of 33 scans (9%) in patients who did not receive furosemide. The SUVmax and SUVmed for the bladder were significantly lower in patients who were pretreated with furosemide (SUVmax, 6.3; SUVmed, 4.6) than patients who were not pretreated with furosemide (SUVmax, 8.8 [P ≤ 0.008]; SUVmed, 6.5 [P ≤ 0.002]). The tumor SUVmax and SUVmed were similar between the patient groups.

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The model would provide a simplified clinical score stratifying the risk of postoperative AKI in patients undergoing aortic surgery.

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Multivariate calibration methods that use fluorescence data for the simultaneous determination of furosemide and triamterene were developed. One of the most salient advantages of them is that the vast amount of information provided by the whole spectrum of the sample is not required. This makes analyses simple and fast. The methods require selecting chemometric parameters such as the specific spectral region and number of factors to be used. Both spectral region and number of factors are selected, simultaneously, by minimising the prediction residual error sum of squares (PRESS). The proposed methods were used for the simultaneous determination of the two drugs in real samples (pharmaceutical preparations) with no excipient separation pre-treatment, with furosemide and triamterene contents of 1.68E-3 to 4.31E-2 and 1.03E-3 to 3.12E-2mugml(-1), respectively; as well as that of triamterene at concentrations of 5.00E-4 to 5.80E-3mugml(-1) in urine samples. The ability to construct the calibration validation sets directly from the urine samples itself avoids the need to consider matrix interferences or to pre-treat the sample and/or separate some analytes The results were quite good in all cases.

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A previously healthy 64-year-old woman attended our hospital with chest pain, facial edema, and general fatigue. A chest radiograph revealed cardiomegaly, small bilateral pleural effusions, and hilar congestion--findings that improved after early therapy with furosemide and methyldigoxin. A chest radiograph recorded 7 years earlier had revealed no dilation of cardiac shadow. There were no findings suggesting atrial septal defect (ASD) or valvular heart disease. Echocardiography revealed a tumor-like mass adhering to the posterior wall of the left atrium. Color-flow Doppler echocardiography revealed a left-to-right shunt at the atrial level. The Qp/Qs ratio as measured by cardiac catheterization was 2.0. Coronary angiography revealed abnormal dilated arteries from the atrioventricular nodal branch and several feeding arteries from the left circumflex branch. We hypothesized that the left-to-right shunt could be due to the tumor, which extended to the rim of the patent foramen ovale, or to the very small, previously unrecognized, ASD. This patient died 6 months after her first admission and an autopsy was performed. Light microscopic examination of the tumor revealed spindle-shaped fibroblast-like cells arranged in a storiform or fascicular pattern. The immunohistochemical findings were consistent with malignant fibrous histiocytoma (MFH). In the literature, left-to-right shunt at the atrial level has not been reported in patients with cardiac MFH.

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Chemical modification of GPb with a T3 derivative allows the development of a simple homogeneous enzyme immunoassay for T3 in unextracted serum.

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Despite advances in medicine, chronic systolic heart failure (CHF) due to hypertension still constitutes a serious clinical challenge.

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Torasemide is a long-acting loop diuretic that combines the effects of both furosemide and spironolactone. It has been reported that torasemide but not furosemide might attenuate myocardial remodeling accompanied by left ventricular (LV) dysfunction. However, nothing is known about the effect of torasemide, long-acting loop diuretic and spironolactone, an aldosterone receptor antagonist in a rat model of chronic heart failure (CHF). Therefore, we compared the therapeutic effects of torasemide, furosemide and spironolactone on the progression of LV remodeling in a rat model of CHF after experimental autoimmune myocarditis (EAM). EAM was elicited in Lewis rats by immunization with porcine cardiac myosin. Twenty-eight days after immunization, rats were treated for 28 days with torasemide, furosemide and spironolactone. Diuretic actions, heart weight/body weight, heart rate, mean blood pressure, myocardial function by echocardiography, cardiac fibrosis, myocyte diameter and cardiac aldosterone synthetase (CYP11B2) were evaluated. Increased cardiac CYP11B2, severe LV remodeling and resultant cardiac dysfunction was found in CHF rats, whereas decreased cardiac CYP11B2, less remodeling and improvement of cardiac function were found in torasemide- and spironolactone-treated CHF rats. Our results indicate that torasemide and spironolactone treatment significantly improved cardiac function and LV remodeling compared with furosemide treatment.

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One of the most challenging dilemmas in pediatric urology today is to determine the optimal management of children with hydronephrotic kidney secondary to suspected ureteropelvic junction obstruction. Some believe in early surgical management while others believe in conservative management. To better define these issues, the authors retrospectively reviewed 101 patients with hydronephrosis.

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Albumin is the main cofactor required by the diuretics tested for direct relaxant action in vitro, and these findings may explain some of the contradictory evidence concerning this action in the literature.

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Calbindin-D28k (CBD-28k) is a calcium binding protein located in the distal convoluted tubule (DCT) and plays an important role in active calcium transport in the kidney. Loop and thiazide diuretics affect renal Ca and Mg handling: both cause Mg wasting, but have opposite effects on Ca excretion as loop diuretics increase, but thiazides decrease, Ca excretion. To understand the role of CBD-28k in renal Ca and Mg handling in response to diuretics treatment, we investigated renal Ca and Mg excretion and gene expression of DCT Ca and Mg transport molecules in wild-type (WT) and CBD-28k knockout (KO) mice. Mice were treated with chlorothiazide (CTZ; 50 mg · kg(-1) · day(-1)) or furosemide (FSM; 30 mg · kg(-1) · day(-1)) for 3 days. To avoid volume depletion, salt was supplemented in the drinking water. Urine Ca excretion was reduced in WT, but not in KO mice, by CTZ. FSM induced similar hypercalciuria in both groups. DCT Ca transport molecules, including transient receptor potential vanilloid 5 (TRPV5), TRPV6, and CBD-9k, were upregulated by CTZ and FSM in WT, but not in KO mice. Urine Mg excretion was increased and transient receptor potential subfamily M, member 6 (TRPM6) was upregulated by both CTZ and FSM in WT and KO mice. In conclusion, CBD-28k plays an important role in gene expression of DCT Ca, but not Mg, transport molecules, which may be related to its being a Ca, but not a Mg, intracellular sensor. The lack of upregulation of DCT Ca transport molecules by thiazides in the KO mice indicates that the DCT Ca transport system is critical for Ca conservation by thiazides.

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lasix medicine 2015-06-17

The resistive index appears to be an Cardura Xl Drug effective parameter for the evaluation and follow-up of unilateral obstructive or nonobstructive ureteropelvic junction dilatation in children.

lasix 2 mg 2015-08-09

Our analysis reveals that the adequate description of PSAC gating Naprosyn Liquid Dosage requires only one exponentially decaying open state, but at least three closed channel states. This model was further supported by single-channel recordings in the presence of furosemide, which inhibits PSAC with moderate affinity through an allosteric mechanism.

lasix oral medication 2017-08-16

In many previous studies, one or the other forebrain circumventricular organ, the subfornical organ (SFO) or organum vasculosum laminae terminalis (OVLT), was lesioned to test whether it was critical for the behavioral or physiological responses to sodium depletion and hypernatremia. These studies conflict in their conclusions. The present study was designed to create discrete lesions of both the SFO and OVLT in the same animals and to compare these with rats having a lesion of only the SFO or OVLT. Both the OVLT-lesioned group and the combined SFO + OVLT-lesioned group drank significantly more water and saline on a daily basis than Controls or SFO-lesioned rats. In both sodium depletion and hypertonic saline testing, rats with SFO lesions displayed transient deficits in salt appetite or thirst responses, whereas the rats with single OVLT lesions did not. In the sodium depletion test, but not in Prandin 5 Mg the hypernatremia test, rats with lesions of both the SFO and OVLT exhibited the largest deficit. The data support the hypothesis that a combined lesion eliminates redundancy and is more effective than a single lesion in sodium depletion tests. The interpretation of the OVLT lesion-only data may have been complicated by a tendency to drink more fluid on a daily basis, because some of those animals drank copious water in addition to saline even very early during the salt appetite test.

lasix dose 2016-09-14

Both intermittent boluses and continuous infusion of frusemide were Voltaren Mg successful in achieving algorithm-driven diuresis. However, continuous infusion therapy was more effective than intermittent boluses since the dose of frusemide required was significantly less.

lasix 20mg cost 2016-08-13

We treated 48 patients with intravenous enalaprilat within 24 hours from the onset of acute myocardial infarction. Concomitant therapy included thrombolytic treatment (29), intravenous metoprolol (34), intravenous nitroglycerin (16) and intravenous furosemide (15). The first 40 patients included had systolic blood pressure at baseline greater than or equal to 110 mmHg. Intravenous bolus injections of 0.2-1.2 mg (mean 1.0 mg) enalaprilat in one hour were given to 20 patients and an intravenous infusion of 1 mg over two hours was administered to another 20 patients, as well as to a separate group of 8 patients with systolic blood pressure between 100-109 mmHg at baseline. The infusion was stopped in five cases when the systolic blood pressure fell below 100 and 90 mmHg, respectively, in the two infusion groups. No hypotensive reactions were symptomatic. Blood pressure decreased from a mean Norvasc Starting Dose of 134/82, 131/79 and 106/72 mmHg to a minimum of 117/71, 118/73 and 97/63 mmHg, respectively, in the three groups. Almost complete suppression of plasma angiotensin converting enzyme activity was achieved within 30 minutes. No significant changes were found in plasma levels of angiotensin II, renin activity or atrial natriuretic peptide between baseline and 24 hours. Treatment was continued with oral enalapril 2.5-10 mg/day, which was generally well tolerated. We conclude that intravenous and oral enalapril added to conventional therapy in the early phase of acute myocardial infarction is well tolerated in selected patients, but should be carefully titrated.

lasix 6 mg 2016-02-01

The role of circulating humoral agents in the pathogenesis of abnormal vascular wall cation composition in benign and malignant renal hypertension was investigated. Male F344 rats with chronic benign (n = 38) and malignant (n = 44) one-kidney, one clip (1K1C) hypertension and normotensive control rats (n = 63) were studied. Malignant hypertension developed spontaneously and was characterized by failure to thrive, weight loss, oedema, renal insufficiency, anaemia or haemoconcentration and hyperkalaemia. For bio-assay, monolayers of quiescent vascular smooth muscle cells from F344 rats were incubated in plasma or plasma extracts of normotensive and hypertensive rats for measurement of labelled rubidium (86Rb) uptake in the presence and absence of 2 mmol/l ouabain and/or 1 mmol/l furosemide. Compared with controls, ouabain-sensitive Rb uptake of cells was reduced in plasma extracts but not in whole plasma of rats with benign hypertension. Ouabain-sensitive Rb uptake was unchanged and ouabain-insensitive Rb uptake Zofran Otc Dosage was reduced in both plasma and plasma extracts of rats with malignant hypertension. The latter was due to a reduction in furosemide-sensitive Rb uptake. In malignant hypertension, the increased sodium (Na) content of the aorta which characterizes benign hypertension was reversed and bladder wall Na content was reduced. The findings suggest that in malignant hypertension a circulating, furosemide-like inhibitor of ouabain-insensitive cation transport is the cause of vascular wall Na depletion and of diuresis and natriuresis that trigger the syndrome.

lasix 8 mg 2015-12-08

Laboratory tests showed moderate to severe hypokalemia with a serum potassium concentration of 2.77 to 3.17 mmol/L, hypomagnesemia (0.31-0.35 mmol/L), hypocalcaemia (1.79-1.99 mmol/L), hypocalciuria (0.12-1.10 mmol/24 h), and metabolic alkalosis. The patient had elevated plasma renin activity and normoaldosteronism; her parathyroid hormone level was normal. Urinary calcium to creatinine ratio was (5.17-23.57) x 10(-3) mg/mg Cr. The renal clearance studies in this patient using furosemide or hydrochlorothiazide disclosed that urine volume and chloride clearance (CCL) Duphaston And Alcohol were increased after furosemide administration, but there was no obvious change after the administration of hydrochlorothiazide. Furthermore, the distal fractional chloride reabsorption [CH2O/(CH2O+CCI)] was dramatically decreased by furosemide administration, whereas thiazide had little effect on it. These findings pointed to the presence of a non-functional thiazide-sensitive sodium/chloride cotransporter in the distal convoluted tubule, so the diagnosis of Gitelman's syndrome (GS) was made.

lasix 711 pill 2016-07-01

This study suggests that nedocromil and furosemide provide a comparable effect in preventing exercise-induced asthma in children. The combined administration of the two drugs significantly Betnovate To Buy increases the protective effects, suggesting a potential therapeutic use.

lasix 80 mg 2017-08-04

Clinical, laboratory, electrocardiographic and echocardiographic data were collected and analyzed for all-cause mortality in 473 furosemide-treated patients aged >or=60 years, hospitalized for acutely decompensated HF.

lasix drug class 2017-08-29

Fischer-344 (F-344) rats avoid NaCl solutions which are preferred by other strains. The present studies examined Na appetite induced by two methods: maintenance on a Na-deficient diet, and Na depletion by injection of furosemide. In comparison with outbred Wistar rats, F-344 rats showed no evidence of Na appetite induced by Na-deficient diet after the first 15 min (study 1) and demonstrated attenuated Na appetite in response to the natriuretic effects of furosemide (study 2). Since Na loss by Wistar and F-344 rats was similar, it is likely that this reduced Na appetite was due to hedonic differences between the strains rather than to differential renal response to furosemide or Na-deficient diet.

lasix brand name 2016-03-20

Interhorse variability with respect to pharmacokinetics of furosemide will result in misclassification of some horses as being in violation of regulatory concentrations.

lasix cost 2016-09-21

We analyzed existing treatment strategies in distressing symptoms after discontinuation of mechanical ventilation.

lasix normal dose 2016-11-08

Frusemide loaded calcium alginate micropellets, an oral microparticulate delivery system, was statistically optimized exhibiting prolonged therapeutic action minimizing its adverse effects.

lasix dosage forms 2017-03-04

Apparent mineralocorticoid excess (AME) is an autosomal recessive disease caused by deficiency of the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2). 11beta-HSD2 converts cortisol into inactive cortisone and prevents the stimulation of the mineralocorticoid receptor by cortisol. In patients with AME, an enhanced stimulation of mineralocorticoid receptors by cortisol in the distal nephron causes an elevated sodium reabsorption and increased potassium excretion. Sodium retention leads to severe low renin hypertension. The diagnosis of AME is based on the detection of an increased concentration of cortisol metabolites and a low or undetectable concentration of cortisone metabolites in urine. Molecular analysis of the HSD11B2 gene confirms the diagnosis. AME is successfully treated by potassium-sparing diuretics, sometimes in combination with loop diuretics (furosemide). Mild forms of AME might occur more frequently than is currently known and should be suspected in patients with hypertension, hypokalemia and decreased plasma renin concentration. Since liquorice can induce the clinical symptoms of AME due to reversible inhibition of the 11beta-HSD2 enzyme by glycyrrhetinic acid, the active ingredient of liquorice, patients suspected of having AME should not consume liquorice.