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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:

Similar Products:
Bumex, Edecrin, Demadex, Sodium Edecrin, Fluss 40


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 user reviews

How to induce most efficiently severe sensorineural hearing loss in mice using a single coadministration of an aminoglycoside antibiotic and a loop diuretic?

lasix 3169 pill

Net secretion from rat intestine of over 3-fold was observed for 20 microM furosemide. Net secretion of furosemide by Caco-2 cells was over 300% greater than for intestinal segments (10-fold vs. 3-fold). For both models, a decrease in furosemide transport in the direction of secretion was observed in the presence of indomethacin (100 microM), although only results using the Caco-2 cells showed in increase in the absorptive transport. Furosemide secretion from Caco-2 cells decreased with decrease in temperature from 37 degrees C to 4 degrees C, suggesting a carrier-mediated process.

lasix dosage elderly

We included in this analysis trials in which preterm infants with or developing chronic lung disease and at least five days of age were all randomly allocated to receive an aerosolized loop diuretic. Eligible studies needed to assess at least one of the outcome variables defined a priori for this systematic review. Primary outcome variables included important clinical outcomes, and secondary outcome variables included pulmonary mechanics and potential complications of therapy.

lasix 50 mg

21 patients with NYHA class III to IV congestive heart failure were randomised to Aldactone (200 mg i.v., 11 pts) or furosemide (20 mg i.v., 10 pts). The mean urine volume in 24 hours in Aldactone group was 1145 ml (range 600 to 2500 ml) and 1678 ml (range 1000 to 3500 ml) in furosemide group (NS). Reduction of magnesium plasma level in furosemide group 24 hours after treatment (from 2.16 +/- 0.18 to 2.01 +/- 0.12 mg/dl, p < 0.05) and slight elevation in Aldactone group (from 1.96 +/- 0.3 to 2.11 +/- 0.18, NS) were observed. Ventricular arrhythmias detected on 24 hour Holter monitoring didn't differ between the study groups.

lasix 10 mg

A total of 23 hypertensive patients with type 2 diabetes and nephropathy were enrolled in this double-blind randomized cross-over trial with four treatment periods, each lasting 2 months. Each patient received placebo and candesartan: 8, 16, and 32 mg daily in random order. Antihypertensive medication was discontinued before enrollment, except for long-acting furosemide, which all patients received throughout the study in median (range) doses of 40 (30-160) mg daily. End points were albuminuria (turbidimetry), 24-h blood pressure (BP) (Takeda-TM2420), and glomerular filtration rate (GFR) (51Cr-labeled EDTA plasma clearance technique).

lasix 8 mg

Progesterone biotransformation was examined in relation to hydroxylating and dehydrogenating enzymes of Cochliobolus lunatus. 11beta-hydroxysteroid dehydrogenase activity (11beta-HSD) was located in cytosolic fraction and was NADP-dependent, inducible by progesterone and apparently uni-directional. Several inhibitors of 11beta-hydroxysteroid dehydrogenase were tested; furosemide, glycyrrhizic-acid and carbenoxolone did not influence the dehydrogenation of 11beta-hydroxy-4-pregnene-3,20-dione to 4-pregnene-3,11,20-trione, although grapefruit juice significantly reduced the rate of progesterone hydroxylation.

lasix drug class

Ouabain-resistant effluxes from pretreated cells containing K+/Na+ = 1.5 into K+ and Na+ free media were measured. Furosemide-sensitive cation effluxes from cells with nearly normal membrane potential and pH were lower in NO3- media than in Cl- media; they were reduced when pH was lowered in Cl- media. When the membrane potential was positive inside furosemide increased the effluxes of Na+ and K+ (7 experiments). With inside-positive membrane potential the furosemide-insensitive effluxes were markedly increased, they decreased with decreasing pH at constant internal Cl- and also when internal Cl- was reduced at constant pH. The correlation between cation flux and the membrane potential was different for cells with high or low internal chloride concentrations. The data with chloride greater than or equal to 47 mM showed a better fit with the single-barrier model than with the infinite number-of-barriers model. With low chloride no significant correlation between flux and membrane potential was found. The data are not compatible with pure independent diffusion of Na+ and K+ in the presence of ouabain and furosemide.

lasix 3 mg

Furosemide is a loop diuretic which has been found to be ototoxic in humans and experimental animals. The ototoxic effects seem to be directed primarily towards the stria vascularis, since its shrinkage and extracellular edema have been observed in correlation with electrophysiologic changes. The present study was designed to examine the interaction of sodium salicylate and furosemide on the cochlear microstructures. Chinchillas weighing 400-600 g were used in all tests performed. The endocochlear potential (EP) was monitored continuously through a microelectrode inserted through the basilar membrane. A control group of animals was injected with 0.5 ml saline intravenously (IV) 30 min before 25 mg/kg furosemide was given. The experimental group of animals was injected with 50 mg/kg sodium salicylate IV 30 min before 25 mg/kg furosemide. The control animals were found to have a mean decrease in EP of 61.1 +/- 7.0 mV. In contrast, the experimental group had very little alteration of the EP following furosemide injection (18.7 +/- 3.9 mV). These findings suggest that sodium salicylate markedly reduces the ototoxic effect of furosemide. This effect may be mediated by an alteration of local or systemic prostaglandin metabolism, or may be due to inhibition of organic acid uptake in the cochlea.

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In patients with congestive heart failure (CHF), use of loop diuretic therapy may result in acute kidney insufficiency (AKI). We assessed the factors that contributed to the development of AKI in patients with CHF treated with loop diuretics in a sample of patients who attended the Cardiovascular Center of Puerto Rico and the Caribbean (CCPRC).

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Acute kidney injury (AKI) is associated with high mortality resulting from extra-renal organ damage, particularly the heart. The present study aimed to investigate the protective effect of sitagliptin, a dipeptidyl peptidase-4 (DPP4) inhibitor, against renal and remote cardiac damage induced by ischemia/reperfusion (IR), a leading cause of AKI. In this attempt, we compared the effects of sitagliptin to furosemide, a loop diuretic. Furosemide is commonly used clinically in AKI however, there is a lack of evidence regarding its beneficial effects in AKI. In addition, the combined administration of both drugs was also investigated. Ischemia was induced in anesthetized male Wistar rats by occluding both renal pedicles for 30min followed by reperfusion for 24h. Sitagliptin (5mg kg(-1)), furosemide (245mg kg(-1)) or their combination were administered orally at 5h post-IR and 2h before euthanasia. Administration of sitagliptin or furosemide ameliorated renal and cardiac deterioration induced by renal IR. This was manifested as significant reduction of serum creatinine, urea, cystatin c, creatine kinase-MB, cardiac troponin-I and lactate dehydrogenase (P<0.05). Drug treatment significantly inhibited IR-induced elevation of TNF-α, NF-κB and caspase-3 (P<0.05) in kidney and heart tissue. In addition, they significantly suppressed malondialdehyde, NO and iNOS content, whereas they increased glutathione and antioxidative enzymes activity (P<0.05) in both tissues. Interestingly, a superior protection was observed with the combination compared to the individual drugs. We assume that this combination represents a promising regimen for managing AKI, particularly with the poor clinical outcome obtained with furosemide alone.

lasix 20mg tab

Infusion of ethanol (20 mmol/L) led to an increase of the intracellular water space by 9.3% +/- 0.4% (n = 3), which was abolished by methylpyrazole and mimicked by acetaldehyde (5 mmol/L). Ethanol-induced cell swelling was completely abolished by bumetanide (5 micromol/L), an inhibitor of Na-K-2Cl cotransport. Ethanol (20 mmol/L) inhibited proteolysis by 18.6% +/- 2.0% (n = 4) in a colchicine-sensitive way. This antiproteolytic effect was quantitatively mimicked by equipotent hyposmotic hepatocyte swelling and by acetaldehyde. Ethanol-induced inhibition of proteolysis was abolished in the presence of methylpyrazole (100 micromol/L), bumetanide (5 micromol/L), furosemide (100 micromol/L), and insulin (35 nmol/L), i.e., conditions that also prevented ethanol-induced cell swelling.

300 mg lasix

The kidneys were evaluated into 2 groups. Group 1 comprised 12 kidneys that had an obstructive curve pattern on Tc-99m EC scans. Group 2 comprised 34 kidneys that had a nonobstructive dilated renogram curve pattern. DRF of the kidneys in each patient were calculated, and the values obtained from the standard and diuretic DMSA scans were compared with each other for all patients and each group. Considering all the patients, the values of mean DRF on both standard and diuretic DMSA images were 55.4%+/-21.2% and 55.4%+/-21.5%, respectively. There were no significant differences between DRF values of each kidney obtained by the 2 methods. When we compared the DRF values in groups 1 and 2, there were again no significant differences. In group 1, the values of mean DRF on standard and diuretic images were 51.7%+/-13.7% and 51.6%+/-13.9%, respectively, and in group 2, the values of mean DRF were 56.7%+/-23.4% and 56.7%+/-23.6%, respectively.

lasix 2 mg

The effect of ibopamine and furosemide in 130 patients with NYHA Class I and II heart failure were studied in a parallel, double-blind, randomized placebo-controlled multi-centre trial. Ibopamine 200 mg b.i.d. was compared to furosemide 40 mg q.d. and placebo. A 1- to 2-week single-blind run-in period was followed by an 8-week double-blind treatment period. Reproducible treadmill exercise test times with the modified Naughton-Balke protocol were required for randomization. Exercise times increased significantly in comparison to the placebo group after 8 weeks of therapy for both the furosemide group (1.2 min, P < 0.035) and the ibopamine group (1.3 min, P < 0.025). Neither furosemide nor ibopamine affected quality of life assessments. Adverse clinical experiences were generally mild and similar in frequency amongst the three treatment groups. The results of this study show the usefulness of both ibopamine and furosemide as monotherapy in patients with mild congestive heart failure.

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A patient presented with advanced cancer of the prostate and underwent bilateral orchiectomy. After 2 years, hypercalcemia developed and was managed successfully with saline diuresis, furosemide, and oral glucocorticoid therapy. It is believed that the patient's hypercalcemia was caused by a metabolic complication of progressive, advanced disease.

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To perform a more critical assessment of infrainguinal vein bypass.

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Trials in which preterm infants with or developing chronic lung disease and at least five days of age were all randomly allocated to receive a loop diuretic either enterally or intravenously were included in this analysis.

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HELEN-II was a randomized clinical trial conducted in Brazil designed to evaluate the clinical efficacy of a nurse-based strategy, started after discharge following an acute decompensated HF (ADHF) admission. HELEN-II compares the efficacy of home visits and telephone reinforcement (n = 123) with that of the conventional strategy, which is based on medical follow-up (n = 129). The primary outcome was a composite endpoint of a first visit to the emergency department (≤ 24 h), a hospital readmission (> 24 h), or all-cause death, assessed during the first 6 months of follow-up. Most enrolled subjects were middle-aged (62 ± 13 years) males (63%) in NYHA functional class II-III (84%) with severe LV dysfunction (mean LVEF 29.6 ± 9%). The primary composite endpoint was decreased by 27% in the interventional group (relative risk 0.73; 95% confidence interval 0.54-0.99; P = 0.049). At the end of follow-up, the rate of use of the standard-of-care HF medications was similar in both groups, except for the higher use of furosemide in the interventional group. Also, HF knowledge and self-care were significantly increased in the interventional group.

lasix 120 mg

During neural development in animals, GABAergic and glycinergic neurons are first excitatory, and then become inhibitory in the mature state. This developmental shift is due mainly to strong expression of the cation-chloride K-Cl cotransporter 2 (KCC2) and down-regulation of Na-K-Cl cotransporter 1 (NKCC1) during maturation. The down-regulation of co-transporter KCC2 after spinal cord transection in animals leads to the depolarising (excitatory) action of GABA and glycine and thus results in a reduction of inhibitory synaptic efficiency. Furosemide, a loop diuretic, has been shown to selectively and reversibly block inhibitory postsynaptic potentials without affecting excitatory postsynaptic potentials in animal spinal neurons. Moreover, this diuretic has been also demonstrated to block the cation-chloride co-transporters. Here, we used furosemide to demonstrate changes in spinal inhibitory networks in healthy human subjects. Non-invasive electrophysiological techniques were used to assess presynaptic inhibition, postsynaptic inhibition and the efficacy of synaptic transmission between muscle afferent terminals and soleus motoneurons in the spinal cord. Orally administered furosemide, at doses commonly used in the clinic (40 mg), significantly reduced spinal inhibitory interneuronal activity for at least 70 min from intake compared to control experiments in the same subjects while no changes were observed in the efficacy of synaptic transmission between muscle afferent terminals and soleus motoneurons. The reduction of inhibition was dose-dependent. Our results provide indirect evidence that reversible changes in the cation-chloride transport system induce modulations of inhibitory neuronal activity at spinal cord level in humans.

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To investigate the diuretic, natriuretic and kaliuretic effects of the antihypertensive Ayurveda drug Karavi Panchaka decoction and compare it with the diuretic frusemide.

3 mg lasix

Acute heart failure is a life-threatening medical emergency, most commonly occurring as an immediate or delayed complication of acute myocardial infarction (AMI), or resulting from severe hypertension or valvular defects (stenosis or incompetence). Occasionally it is caused by patients' non-compliance with medication orders. In this case the patient had a history of three previous AMIs, controlled hypertension, and controlled congestive heart failure (CHF) for which he took two 40 mg frusemide tablets (a very potent oral diuretic) each morning. Because he had experienced bladder discomfort during the latter stages of previous appointments he decided to delay taking the diuretic until after his appointment and acute heart failure ensued.

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Furosemide, either alone or in combination with captopril, is capable to prevent myocardial calcification, cardiac hypertrophy and hypertension, maintaining blood Ca(2+) and phosphate levels by slowing CRF.

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Azosemide provided better prognosis in heart failure rats compared with furosemide, partly through attenuation of the reflex increase in cardiac sympathetic neuronal activity caused by the development of heart failure. The current findings suggest a need for clinical trials examining whether long- and short-acting diuretics provide a different prognosis in patients with heart failure.

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Furosemide, a loop diuretic, is used to increase urine output in patients with acute kidney injury (AKI). It remains uncertain whether the benefits of furosemide in AKI outweigh its potential harms. We investigated if furosemide influenced oxidative stress in 30 critically ill patients with AKI by measuring changes in F2-isoprostanes (F2-IsoPs), markers of in vivo oxidative stress, in plasma and urine following intravenous furosemide. Urine F2-IsoPs were higher in sepsis (p = 0.001) and increased in proportion to urine furosemide (p = 0.001). The furosemide-induced increase in urine F2-IsoPs differed depending on AKI severity (p < 0.001) and was greatest in those with the most severe AKI. Furosemide had no effect on plasma F2-IsoPs. We demonstrate for the first time that furosemide increases renal oxidative stress in AKI and find that patients with the most severe AKI-to whom the largest doses are likely to be administered-showed the greatest increase in oxidative stress. These findings lead to the hypothesis that the common practice of administering high-dose furosemide to convert oliguric to nonoliguric AKI may induce harmful oxidative stress in the kidneys, and an adequately powered, randomized controlled trial is required to determine if clinical benefits of this dosing strategy justify its potential harms. Antioxid. Redox Signal. 26, 221-226.

lasix oral dosage

This case demonstrates the effect of exercise on the clearance of Tc-99m MAG3 in a patient with renal insufficiency status post-liver transplant. Even after furosemide administration, the tracer was retained in the kidneys after exercise. This is in contrast to normal clearance demonstrated on a baseline study performed 3 days previously.

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To determine changes in RAS activation and clinical correlates following furosemide withdrawal in elderly heart failure patients without left ventricular systolic dysfunction.

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The experiments on rats showed that the dietary mineral composition influences renal circulation and saluretic function and modifies the related effects of furosemide. In particular, a high NaCl intake reduces the blood perfusion in the renal cortex and increased that in the renal medulla, thus increasing sodium excretion with urine. The use of hyposol, a table salt substituent, enhances the blood flow in the renal medulla and leads to a significant increase in the diuresis, natriuresis, and kaliuresis. Furosemide (10 mg/kg) sharply increases the medullar circulation and electrolyte excretion on the background of standard diet. However, these effects were much less pronounced on the background of hypersodium diet or hyposol administration.

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lasix 30 mg 2016-03-09

Furosemide-sensitive Na-K cotransport was measured as zero-trans efflux of each ion from fresh or Na loaded erythrocytes in normotensives (n = 34), essential (n = 41) or secondary (n = 12) hypertensives and essential (n = 17) or secondary (n = 5) hypotensives. The stoichiometry of Na and K efflux was 0.9:1 in fresh cells and 1:1 in cells loaded with sufficient Na to give near the maximum velocity (Vmax) in a combined analysis. There buy lasix was a tendency toward a negative correlation between the Vmax of Na efflux and serum total cholesterol (p = 0.09) in the whole and it was significant in normotensives (r = -0.60). Vmax of Na efflux also negatively correlated to age (p less than 0.01). After adjustment for age and total cholesterol level, essential hypertensives had a significantly (p less than 0.01) higher mean Vmax of Na efflux (0.657 +/- 0.029 mM/l cells/hr) than normotensives (0.388 +/- 0.045), while essential hypotensives had a lower value (0.212 +/- 0.047) (p less than 0.01). Na efflux from fresh cells adjusted for internal Na content was higher in essential hypertensives (0.173 +/- 0.018) than in normotensives (0.107 +/- 0.026) (p less than 0.05). Thus, elevated cotransport was linked to essential hypertension and reduced cotransport to hypotension. Whether it is a cause or a result remains to be further investigated.

lasix 40mg tab 2015-10-23

We reviewed our experience with buy lasix 53 newborns who had unilateral hydronephrosis presumed secondary to ureteropelvic junction obstruction. We divided the patients according to the presence of mild hydronephrosis and no obstruction on a furosemide renogram, severe hydronephrosis and obstruction on a furosemide renogram or a unilateral multicystic kidney.

tab lasix 5mg 2015-03-21

AVP-induced alterations of rBSC1 expression, as well as those of AQP2, are involved in the pathogenesis of SIADH. The pharmacologic blockade of AVP stimulus in SIADH limits its therapeutic efficacy by discontinuing the vasopressin escape, and buy lasix the selective inhibition of rBSC1 complements this limitation.

lasix dosage elderly 2016-03-26

The standard model is unlikely to be correct and the Homsy sign is probably an artefact seen buy lasix in patients with impeded urinary drainage. Computer modelling of individual renograms is feasible and can provide useful insights into the pathophysiology of renal uptake and drainage.

lasix 10mg tablet 2016-03-10

Our purpose was to assess the effects of the adjunctive use of cardiovascular buy lasix dynamics monitoring in the ambulatory management of 199 pregnant patients with severe hypertension.

lasix dosage racehorses 2015-08-15

Thirty-six adult patients with cardiogenic pulmonary edema (CPA) with unresolving dyspnea, respiratory rate above 30/min and/or SpO2 above buy lasix 90% with O2 higher than 10 l/min despite conventional therapy with furosemide and nitrates.

lasix drug 2016-03-21

We enrolled 98 patients with CHF who were receiving furosemide and an angiotensin-converting enzyme inhibitor, and they were randomly divided into furosemide (n=49) and azosemide (n=49 buy lasix ) groups. The furosemide group continued furosemide at the same dosage, and the azosemide group switched from furosemide to azosemide. At baseline and after 3 months, we measured body weight, and levels of brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), norepinephrine, active renin, creatinine, blood urea nitrogen, sodium, potassium, and hematocrit. Chest X-ray and echocardiography were also performed.

lasix buy online 2016-11-25

Renal US and CT revealed bilateral nephrocalcinosis of the medullary pyramids in 15 (83.3%) out of 18 patients. The duration of furosemide abuse was similar between nephrocalcinosis positive (NC(+)) and nephrocalcinosis negative (NC(-)) groups. The daily dose of furosemide was nearly 10 times higher buy lasix in the NC(+) group (range 120-2800 mg, mean 538 mg) than the NC(-) group (range 40-80 mg, mean 67 mg). All patients showed variable degrees of renal insufficiency and there was no difference in creatinine clearance between the NC(+) and NC(-) groups (P>0.05). Kidney biopsies performed in three patients showed focal tubulo-interstitial fibrosis and atrophy and calcifications were observed in outer medullary tubulo-interstitium.

lasix 75 mg 2017-08-09

We reviewed the medical records of patients with hypertensive emergencies admitted to the medical wards of Siriraj Hospital in 2003 and collected data buy lasix on their characteristic, management, investigations, and follow-ups through 31 December 2007.

lasix mg 2016-08-06

We describe a case of vinorelbine tartrate (VNR) associated acute respiratory failure. A 65-year-old man with non-small cell lung cancer developed acute respiratory failure 50 minutes after his first infusion with VNR in combination with mitomycin-C. The patient was treated with furosemide, dopamine and high-dose methylprednisolone, and recovered with no discernible sequelae. Although clinical trials have shown that respiratory symptoms buy lasix associated with VNR treatment have only rarely been observed and the putative mechanism remains to be elucidated, patients receiving VNR should be monitored carefully, particularly in the first few hours after intravenous administration.

lasix 240 mg 2017-01-27

Six Sprague-Dawley rats were administered with STZ to induce diabetes (group 1). R2* was measured buy lasix before, during, and after administration of iodixanol. R2* readings were sampled from 4 renal regions: inner medulla, inner stripe of outer medulla (ISOM), outer stripe of outer medulla, and cortex. Peak R2* and initial upslope of R2* increase after iodinated contrast were calculated. Data from 12 nondiabetic rats pretreated with nitric oxide synthase and prostaglandin inhibitors to induce susceptibility to contrast-induced acute kidney injury (pretreatment model) from a previous study were reanalyzed for peak R2* and initial upslope of R2* increase after contrast. Six of these animals received saline (group 2), and the other 6 received furosemide (group 3) before iodixanol.

lasix tabs 2017-07-23

In the spinal pithed rat, DuP 753, 2-n-butyl-4-chloro-5-hydroxy-methyl buy lasix -1-[(2'-(1H-tetrazol-5-yl)biphe nyl-4-yl) methyl] imidazole potassium salt, inhibited competitively the pressor response to angiotensin II (AII), whereas saralasin showed a noncompetitive pattern of interaction. It did not alter the pressor responses to vasopressin and norepinephrine as well as the heart rate response to isoproterenol. In the anesthetized rat, DuP 753 did not affect the vasodepressor response to bradykinin. Given p.o. or i.v., DuP 753 did not lower blood pressure in conscious normotensive rats, but it inhibited the pressor response to AII but not to vasopressin. It lowered blood pressure in furosemide-treated normotensive rats. Unlike saralasin, DuP 753 did not cause a transient increase in blood pressure even at 100 mg/kg i.v. DuP 753 at 3.5 micrograms i.c.v. inhibited the pressor response to i.c.v. AII, whereas DuP 753 at 10 mg/kg p.o. did not, suggesting that a single p.o. administration of DuP 753 does not affect brain AII receptors which are accessible by i.c.v. injection. Our study indicates that DuP 753 is a p.o. active, nonpeptide, selective, competitive AII receptor antagonist.

lasix 5 mg 2016-08-26

Treatment with inhaled lysine buy lasix acetylsalicylate and furosemide allows a considerable sparing of inhaled steroids without significant side effects in patients with severe asthma.

300 mg lasix 2015-10-17

In this study, we compare cholesterol levels during the first year after renal transplantation in FK506 (Prograf)- and cyclosporine-treated patients matched for cumulative first-year steroid dose and hypercholesterolemia risk factors. All patients had pretransplant cholesterol levels < 200 mg/dl. At 3 months posttransplant, 68% of the cyclosporine-treated patients had at least one cholesterol level greater than 200 mg/dl compared with 30% of the FK506-treated patients (P < 0.05). At the end of the year, 26% of FK506- and 67% of cyclosporine-treated patients buy lasix remained hypercholesterolemic (P < 0.05). We conclude that cyclosporine has inherently more effect on cholesterol levels than FK506 during the first year after kidney transplantation.

lasix drug interactions 2017-09-24

Kidney transplant rejection may be accompanied by defective urinary acidification. Its pathogenesis is unknown. There are shared histologic features between kidney transplant rejection and the distal renal tubular acidosis (RTA) of Sjogren syndrome, which led us to hypothesize that deficient collecting duct H+ adenosine triphosphatase (ATPase) expression--which is lacking in the RTA of Sjogren syndrome - may cause the RTA of kidney transplant rejection. Six kidney transplant recipients with biopsy evidence for rejection and two control subjects were studied physiologically and by immunohistochemistry. We found defective urinary acidification in all 6 kidney transplant patients. Ammonium excretion was diminished in relation to the degree of azotemia. There was an abnormal response to furosemide in all 6, suggesting distal tubular dysfunction. Distal H+ ATPase staining was reduced in relation to the degree of azotemia, although it was not totally absent even in the worst case. This was paralleled Buspar 75 Mg by the urinary PCO2 response. Both control subjects had good urine PCO2 and H+ ATPase staining and adequate urine pH response to furosemide. They had reduced urinary ammonium (NH4) concentrations in relation to modest azotemia. We conclude that kidney transplant rejection may be accompanied by defective urinary acidification, which is not primarily due to a lack of H+ ATPase. The RTA of kidney transplant rejection appears to result from defective ammonium excretion, generalized distal tubular malfunction, and--in severe cases--from a reduction in distal nephron H+ ATPase expression.

lasix oral dosage 2016-10-18

Our single channel work has characterized two ion channels capable of depolarizing mesangial cells and activating classic, voltage-activated Ca2+ channels in response to growth-stimulatory peptides (such as Ang II, ET and insulin): (1) Ca(2+)-dependent, 4 pS Cl- channel promoting Cl- efflux; and (2) Ca(2+)-dependent, 27 pS nonselective cation channels promoting cation influx. We have also characterized a third channel which provides an alternative, receptor-operated pathway for Ca2+ Desyrel 30 Mg entry in response to the growth factor, PDGF: (3) Ca(2+)-permeable, 1 pS cation channel. Consistent with our model of mesangial cell signal transduction (Fig. 1), these three mesangial cell ion channels are activated by binding of growth factors to membrane receptors (Fig. 8). Defective channel regulation, such as occurs in early diabetes mellitus, would promote mesangial cell relaxation and pathogenic glomerular hyperfiltration. Glomerular hyperfiltration and hypertension have been proposed to be major pathogenic factors in renal disease progression [4, 29, 38, 39]. Compensatory renal growth factor responses initially provide adaptive changes in glomerular hemodynamics after loss of functional renal mass. However, chronic stimulation of these mesangial cell ion channels by renal growth factors would promote sustained extracellular Ca2+ entry, resulting in mesangial cell contraction and growth, and progressive decreases in Kf and GFR. Eventually, this process leads to irreversible renal damage due to the development of glomerulosclerosis and interstitial fibrosis.

lasix tablets 2016-06-28

A cross-sectional study of Duphaston Syrup blood thiamine and thiamine ester concentrations.

lasix 120 mg 2016-02-24

Blood pressure (BP) was measured every 5 min with the use of an automatic oscillometric device. Serum lactate, PO2, pH value, and base excess (BE) were evaluated on admission and 6 h later. Blood pressure, serum lactate and BE on admission were significantly lower (SBP: 155 +/- 30 vs 179 +/- 33 mm Hg; p = 0.0002; DBP: 82 +/- 17 vs 93 +/- 19 mmHg; p = 0.001; lactate: 2.2 +/- 1.6 vs 3.9 +/- 2.7; p = 0.0001; BE: -1.9 +/- 3.9 vs -4.4 +/- 1.7; p = 0.0005) and PO2 and pH values were significantly higher in Levitra Dosage Instructions the urapidil group compared to the nitroglycerin group (PO2: 75 +/- 25 vs 66 +/- 17; p = 0.036; pH: 7.33 +/- 0.08 vs 7.29 +/- 0.09; p = 0.042). After 6 h no differences between the two groups were observed.

lasix 20 mg 2017-06-15

The counterfeiting of pharmaceuticals has been detected since about 1990 and has alarmingly continued to pick up steam. We have been recently involved in an evaluation program of some of the most commonly prescribed cardiovascular drugs in Africa, for analysing an important number of tablets or capsules obtained from different places in seven African countries. A reversed-phase high-performance liquid chromatography with tandem mass spectrometry method was developed and validated to simultaneously control the identity and the quantity of acenocoumarol, amlodipine, atenolol, captopril, furosemide, hydrochlorothiazide and simvastatin in tablets. Their separation was performed on a Kinetex® C(18) (100 mm × 2.1 mm inside diameter, 2.6 μm) column using a gradient elution of 20 mM ammonium formate buffer and acetonitrile (90:10 10:90 v/v) at a flow rate Stromectol 6mg Tablet of 0.5 mL/min. The analytes were detected using electrospray ionisation tandem mass spectrometry in both positive and negative modes with multiple reaction monitoring. Tandem mass spectrometry fragmentation patterns of captopril, furosemide and acenocoumarol, up to now not detailed in the literature, were also studied to assist in the selection of the most relevant transitions towards the objectives. The developed method was validated as per International Conference on Harmonisation guidelines with respect to specificity, linearity, trueness, precision, limits of detection and quantification. It has been successfully applied to the control of oral forms of seven cardiovascular drugs collected in African countries.

lasix brand name 2017-12-01

We studied the effects of hypertonic stress on ion transport and cell volume regulation (regulatory volume increase; RVI) in the human tumor cell-line HepG2. Ion conductances were monitored in intracellular current-clamp measurements with rapid ion-substitutions and in whole-cell patch-clamp recordings; intracellular pH buffering capacity and activation Flagyl S Dosage of Na(+)/H(+) antiport were determined fluorometrically; the rates of Na(+)-K(+)-2Cl(-) symport and Na(+)/K(+)-ATPase were quantified on the basis of time-dependent and furosemide- or ouabain-sensitive (86)Rb(+) uptake, respectively; changes in cell volume were recorded by means of confocal laser-scanning microscopy. It was found that hypertonic conditions led to the activation of a cation conductance that was inhibited by Gd(3+), flufenamate as well as amiloride, but not by benzamil or ethyl-isopropyl-amiloride (EIPA). Most likely, this cation conductance was non-selective for Na(+) over K(+). Hypertonic stress did not change K(+) conductance, whereas possible changes in Cl(-) conductance remain ambiguous. The contribution of Na(+)/H(+)antiport to the RVI process appeared to be minor. Under hypertonic conditions an approximately 3.5-fold stimulation of Na(+)-K(+)-2Cl(-)symport was observed but this transporter did not significantly contribute to the overall RVI process. Hypertonic stress did not increase the activity of Na(+)/K(+)-ATPase, which even under isotonic conditions appeared to be working at its limit. It is concluded that the main mechanism in the RVI of HepG2 cells is the activation of a novel non-selective cation conductance. In contrast, there is little if any contribution of K(+) conductance, Na(+)/H(+) antiport, Na(+)-K(+)-2Cl(-) symport, and Na(+)/K(+)-ATPase to this process.

lasix 80mg tab 2017-04-09

Three hundred and sixty one patients were included in this study. The prevalence of WRF among those who met the inclusion criteria was 40.2%. In the majority of cases, WRF started within the first 48 hrs of admission. Analysis of data indicated that eight variables were significantly associated with WRF: renal dysfunction (P< 0.0001), diabetes mellitus (P= 0.005), hypertension (HTN) (P< 0.0001), congestive heart failure (CHF) (P= 0.021), elderly (being > 65 years) (P= 0.003), number of diagnosis (P< 0.001), furosemide (P = 0.001) and calcium channel blockers (P= 0.01 Protonix Gtt Dosing ) administration at admission. Regression analysis indicated that HTN (P =0.033) and renal dysfunction (P= 0.007) were predictors of WRF in model I, while furosemide administration (P= 0.01) was the only predictor of WRF in model II.

lasix drug class 2015-09-10

Study subjects ranged from 2-46 months of age, were fluid overloaded, and were receiving a continuous infusion of furosemide (> or =6 mg/kg/day). Patients with hemodynamic instability or liver dysfunction were excluded.

lasix online 2015-12-08

The blockade of the lateral parabrachial nucleus (LPBN) with GABA(A) receptor agonist muscimol induces robust hypertonic NaCl and water intake by rats. In the present study we investigated the effects of previous injections of losartan (AT(1) angiotensin receptor antagonist) into the LPBN on 0.3M NaCl and water intake induced by muscimol injected bilaterally in the same area in fluid replete rats and in rats treated with the diuretic furosemide combined with a low dose of the angiotensin-converting enzyme inhibitor captopril injected subcutaneously. Male Wistar rats with stainless steel cannulas implanted bilaterally into the LPBN were used. Bilateral injections of muscimol (0.5 nmol/0.2 μl, n=8) into the LPBN in fluid replete rats induced 0.3M NaCl intake (23.4±4.1 vs. saline: 0.4±0.4 ml/3h) and water intake (9.3±1.9 vs. saline: 0.7±0.4 ml/3h) and pre-treatment of the LPBN with losartan (50 μg/0.2 μl) reduced 0.3M NaCl intake (3.3±2.5 ml/3h) and water intake (4.0±2.9 ml/3h) induced by muscimol. In rats treated with furosemide+captopril, pre-treatment with losartan into the LPBN attenuated the increase of 0.3M NaCl intake produced by muscimol (12.8±5.3, vs. saline+muscimol: 36.7±6.7 ml/3h) without changing water intake. Therefore, the results suggest that deactivation of LPBN inhibitory mechanisms by muscimol injections into the LPBN is facilitated by endogenous angiotensin II acting on AT(1) receptors in the LPBN, which drives rats to ingest large amounts of hypertonic NaCl.

lasix medication 2015-06-02

Focus groups are an effective and efficient method to explore patients opinions of barriers to drug therapy adherence. Such information can have a direct impact on management of patients with CHF. Information gathered in this study will be used to construct a survey to measure barriers to drug adherence and design interventions to improve adherence.

lasix 500mg tablet 2015-02-07

1. Frusemide is removed from the body by biotransformation and renal secretion, but since frusemide metabolism is not altered in patients with hepatic cirrhosis, the role of the liver may be questioned. The aim of the study was to investigate which organs contribute to the first-pass metabolism and systemic clearance of frusemide. 2. Groups of anaesthetized New Zealand rabbits were administered frusemide proximally (prox) and distally (dist) to different organs, and blood was sampled from the abdominal aorta. The area under frusemide plasma concentrations-time curve (AUC0-infinity) was calculated and frusemide extraction by an organ was estimated from the ratio (AUCdist-AUCprox)/AUCdist. The small intestine extracted 83% of the absorbed dose of frusemide but the first-pass uptake by the liver and lungs was negligible. 3. To assess the contribution of the intestine and the kidneys to the systemic clearance of frusemide, it was injected into the jugular vein and blood was sampled proximal and distal to each organ. The kidneys extracted 24% of frusemide circulating in the renal arteries; on the other hand, the ability of the intestine to extract frusemide from the systemic circulation could not be detected. 4. The lungs did not metabolize frusemide in vitro; the rate of metabolism of frusemide in vitro by kidneys was similar to that estimated in the intestine, and both rates were faster (P < 0.05) than that observed in the liver. 5. It is concluded that in rabbits, presystemic metabolism of frusemide is carried out by the intestine, and that systemic clearance of frusemide is mainly performed by the kidneys, although other organs, such as the intestine and the liver, must contribute to it.

lasix 70 mg 2015-03-31

In patients hospitalized with heart failure, oral tolvaptan in addition to standard therapy including diuretics improved many, though not all, heart failure signs and symptoms, without serious adverse events.

lasix medicine 2017-11-14

We conducted blinded clinical trials on patients with ST-elevation myocardial infarction (STEMI) and monitored whether the condition would progress to APE. ITI was measured non-invasively by the Edema Guard Monitor (EGM, model RS-207) every 30 min. The measurement threshold for the diagnosis of APE was fixed at > 12% decrease in ITI from baseline as described in our methodology. The patients were divided into one group that received standard treatment after the appearance of clinical signs of APE without considering the prediction of APE by EGM devise (Group 1), and another group of asymptomatic patients in whom development of APE was predicted by using only EGM measurements (Group 2). The latter participants' PT consisted of furosemide, intravenous nitroglycerine and supplemental oxygen.