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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.

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Within-subject variability in MFBIA at 1, 5, 50, and 100 kHz expressed as standard deviations was 21, 19, 14, and 14 Ohm (omega), respectively. Furosemide caused a mean weight loss of 1.8 +/- 0.6 kg, which resulted in significant increases in impedance of 57 +/- 24 omega at 1 kHz and 37 +/- 12 omega at 100 kHz (p < .001). The responsiveness of MFBIA for the diuretic intervention was best at 5 kHz (responsiveness index = 1.98).

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Urinary output increased significantly and urinary osmolality decreased after oral administration of Sclederma of Poria cocos (hoelen) for both 1 and 4 weeks. Sclederma of Poria cocos (hoelen) caused less electrolyte disorder than furosemide. Furthermore, Sclederma of Poria cocos (hoelen) reduced the levels of plasma BNP in CHF rats, whereas furosemide had no effect. Importantly, both mRNA and protein expression of AQP2 were down-regulated and urinary excretion of AQP2 was decreased after administration of Sclederma of Poria cocos (hoelen) to CHF rats. Similarly, Sclederma of Poria cocos (hoelen) reduced plasma arginine vasopressin (AVP) level and down-regulated vasopressin type 2 receptor (V2R) mRNA expression.

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We analysed the clinical significance of WRF in 318 consecutive patients admitted at our institute for AHF. WRF was defined as the occurrence, at any time during the hospitalisation, of both a > or =25% and a > or =0.3 mg/dL increase in serum creatinine (s-Cr) from admission (WRF-Abs-%).

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More than a third of patients who received prehospital furosemide did not have an HF diagnosis, suggesting that the prehospital diagnosis of HF can be challenging. Serious adverse outcomes were identified in all patient groups and we found no statistically significant associations between furosemide use and adverse events.

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PTHrP was elevated and no evidence of a malignancy was found. Treatment consisting of a low-calcium CalciLo diet (in place of breast milk) adequately controlled the patient's hypercalcaemia. Hypercalcaemia associated with CAKUT in infancy is not all that uncommon and was reported in 15/99 infants in another study, most of whom had a suppressed PTH similar to that of our patient. PTHrP was not measured in these cases and may have also been elevated.

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A Fourier transform infrared derivative spectroscopy (FTIR-DS) method has been developed for determining furosemide (FUR) in pharmaceutical solid dosage form. The method involves the extraction of FUR from tablets with N,N-dimethylformamide by sonication and direct measurement in liquid phase mode using a reduced path length cell. In general, the spectra were measured in transmission mode and the equipment was configured to collect a spectrum at 4 cm(-1) resolution and a 13 s collection time (10 scans co-added). The spectra were collected between 1400 cm(-1) and 450 cm(-1). Derivative spectroscopy was used for data processing and quantitative measurement using the peak area of the second order spectrum of the major spectral band found at 1165 cm(-1) (SO2 stretching of FUR) with baseline correction. The method fulfilled most validation requirements in the 2 mg/mL and 20 mg/mL range, with a 0.9998 coefficient of determination obtained by simple calibration model, and a general coefficient of variation <2%. The mean recovery for the proposed assay method resulted within the (100±3)% over the 80%-120% range of the target concentration. The results agree with a pharmacopoeial method and, therefore, could be considered interchangeable.

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The severity of acute kidney injury, as reflected by the measured creatinine clearance, alters both pharmacokinetics and pharmacodynamics of furosemide in acute kidney injury, and was the only reliable predictor of the urinary output response to furosemide in acute kidney injury.

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The effect of extracellular and intracellular Na+ (Nao+, Nai+) on ouabain-resistant, furosemide-sensitive (FS) Rb+ transport was studied in human erythrocytes under varying experimental conditions. The results obtained are consistent with the view that a (1 Na+ + 1 K+ + 2 Cl-) cotransport system operates in two different modes: mode i) promoting bidirectional 1:1 (Na+-K+) cotransport, and mode ii) a Nao+-independent 1:1 ki+ exchange requiring Nai+ which, however, is not extruded. The activities of the two modes of operation vary strictly in parallel to each other among erythrocytes of different donors and in cell fractions of individual donors separated according to density. Rb+ uptake through Rbo+/Ki+ exchange contributes about 25% to total Rb+ uptake in 145 mM NaCl media containing 5 mM RbCl at normal Nai+ (pH 7.4). Na+-K+ cotransport into the cells occurs largely additive to K+/K+ exchange. Inward Na+-Rb+ cotransport exhibits a substrate inhibition at high Rbo+. With increasing pH, the maximum rate of cotransport is accelerated at the expense of K+/K+ exchange (apparent pK close to pH 7.4). The apparent KmRbo+ of Na+-K+ cotransport is low (2 mM) and almost independent of pH, and high for K+/K+ exchange (10 to 15 mM), the affinity increasing with pH. The two modes are discussed in terms of a partial reaction scheme of (1 Na+ + 1 K+ + 2 Cl-) cotransport with ordered binding and debinding, exhibiting a glide symmetry (first on outside = first off inside) as proposed by McManus for duck erythrocytes (McManus, T.J., 1987, Fed. Proc., in press). N-ethylmaleimide (NEM) chemically induces a Cl--dependent K+ transport pathway that is independent of both Nao+ and Nai+. This pathway differs in many properties from the basal, Nao+-independent K+/K+ exchange active in untreated human erythrocytes at normal cell volume. Cell swelling accelerates a Nao+-independent FS K+ transport pathway which most probably is not identical to basal K+/K+ exchange. Ko+ less than Nao+ less than Lio+ less than Mgo2+ reduce furosemide-resistant Rb+ inward leakage relative to cholineo+.

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Apocynin (NADPH oxidase inhibitor) normalized superoxide production and ouabain-sensitive O2 consumption and furosemide-sensitive O2 consumption by mTALs from STZ rats, without altering O2 consumption by mTALs from sham rats. Apocynin also unmasked a T1D-induced increase in nitrite production. NOS inhibition did not alter superoxide production in either group. In sham mTAL, total NOS inhibition, but not isoform-specific inhibition of NOS1 or NOS2, increased ouabain- and furosemide-sensitive O2 consumption, confirming a tonic inhibitory impact of NOS3 on sodium transport. In contrast, neither total nor isoform-specific NOS inhibition altered O2 consumption by STZ mTAL. Apocynin treatment of STZ mTAL unveiled the ability of isoform-specific NOS inhibition to significantly increase O2 consumption, without further increase in O2 consumption with total NOS inhibition.

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The pharmacodynamics of 1 or 2 mg/kg of furosemide administered as a single dose orally or intravenously were studied in 34 hospitalized children (ranging in age from 9 days to 16.5 years) with normal renal function. These patients were divided into 3 groups: infants (furosemide 1 mg/kg, intravenously); children with steroid-responsive nephrotic syndrome (furosemide 2 mg/kg, orally and intravenously); patients with urinary tract infections and mild hypertension (furosemide 2 mg/kg, orally). A statistically significant positive linear relationship was found in these groups between the furosemide urinary excretion rate and urine flow rate, but log dose-response curves to furosemide were found to vary between the groups of patients studied. This variability reflects differences in the relationship between the amounts of furosemide reaching active sites and the pharmacodynamic effect of the drug. No sigmoid-shaped log dose-response curve (i.e., one approaching a zero response at very low furosemide urinary excretion rates, and a maximum response at very high excretion rates) was attained in this study. This suggests that the capacity of the kidney tubules to respond diuretically to the administered doses of furosemide was not exceeded in the studied patients. However, in the infants, a very steep log dose-response curve to a 1 mg/kg intravenous dose of furosemide suggests that higher doses may not result in a significant increase in diuretic response in infants with reasonably normal renal function. The lowest mean furosemide urinary excretion rate associated with significant diuresis was 0.58 +/- 0.33 micrograms/kg/min. Also, a significant correlation was found between the amount (in milligrams), of furosemide excreted in the urine during the first 6 h after administration and the urine volume collected during that time (r = 0.71; p less than 0.001; number of measurements = 43).

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Furosemide infusion therapy was associated with moderately negative cumulative fluid balances, electrolyte shifts, and mild transient worsening of renal function.

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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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The equilibrium potential (E(GABA)(-PSC)) for gamma-aminobutyric acid (GABA) A receptor mediated inhibitory postsynaptic currents (PSCs) in hippocampal CA1 pyramidal neurons shifts when theta-burst stimulation (four pulses at 100 Hz in each burst in a train consisting of five bursts with an inter-burst interval of 200 ms, the train repeated thrice at 30-s intervals) is applied to the input. E(GABA)(-PSC) is regulated by K(+)/Cl(-) co-transporter (KCC2). GABA(B) receptors are implicated in modulating KCC2 levels. In the current study, the involvement of KCC2, as well as GABA(B) receptors, in theta-burst-mediated shifts in E(GABA)(-PSC) was examined. Whole-cell patch recordings were made from hippocampal CA1 pyramidal neurons (from 9 to 12 days old rats), in a slice preparation. Glutamatergic excitatory postsynaptic currents were blocked with dl-2-amino-5-phosphonovaleric acid (50 microM) and 6,7-dinitroquinoxaline-2,3-dione (20 microM). The PSC and the E(GABA)(-PSC) were stable when stimulated at 0.05 Hz. However, both changed following a 30-min stimulation at 0.5 or 1 Hz. Furosemide (500 microM) and KCC2 anti-sense in the recording pipette but not bumetanide (20 or 100 microM) or KCC2 sense, blocked the changes, suggesting KCC2 involvement. Theta-burst stimulation induced a negative shift in E(GABA)(-PSC), which was prevented by KCC2 anti-sense; however, KCC2 sense had no effect. CGP55845 (2 microM), a GABA(B) antagonist, applied in the superfusing medium, or GDP-beta-S in the recording pipette, blocked the shift in E(GABA)(-PSC). These results indicate that activity-mediated plasticity in E(GABA)(-PSC) occurs in hippocampal CA1 pyramidal neurons and theta-burst-induced negative shift in E(GABA)(-PSC) requires KCC2, GABA(B) receptors and G-protein activation.

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We sought to determine the effect of aspirin on the venodilator effect of furosemide in patients with chronic heart failure (CHF) BACKGROUND: Furosemide has an acute venodilator effect preceding its diuretic action, which is blocked by nonsteroidal anti-inflammatory, drugs. The ability of therapeutic doses of aspirin to block this effect of furosemide in patients with CHF has not been studied. For comparison, the venodilator response to nitroglycerin (NTG) was also studied.

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Liver cirrhosis is often complicated by an impaired renal excretion of water and sodium. Diuretics tend to further deteriorate renal function. It is unknown whether chronic selective adenosine A(1) receptor blockade, via inhibition of the hepatorenal reflex and the tubuloglomerular feedback, might exert diuretic and natriuretic effects without a reduction of the glomerular filtration rate. In healthy animals intravenous treatment with the novel A(1) receptor antagonist SLV329 resulted in a strong dose-dependent diuretic (up to 3.4-fold) and natriuretic (up to 13.5-fold) effect without affecting creatinine clearance. Male Wistar rats with thioacetamide-induced liver cirrhosis received SLV329, vehicle or furosemide for 12 weeks. The creatinine clearance of cirrhotic animals decreased significantly (-36.5%, p<0.05), especially in those receiving furosemide (-41.9%, p<0.01). SLV329 was able to prevent this decline of creatinine clearance. Mortality was significantly lower in cirrhotic animals treated with SLV329 in comparison to animals treated with furosemide (17% vs. 54%, p<0.05). SLV329 did not relevantly influence the degree of liver fibrosis, kidney histology or expression of hepatic or renal adenosine receptors. In conclusion, chronic treatment with SLV329 prevented the decrease of creatinine clearance in a rat model of liver cirrhosis. Further studies will have to establish whether adenosine A(1) receptor antagonists are clinically beneficial at different stages of liver cirrhosis.

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A possible role for loop diuretic-sensitive Cl-/cation cotransport in volume regulation in the pancreatic beta-cells was investigated by measuring 86Rb+ efflux from beta-cell-rich pancreatic islets as well as the size of isolated beta-cells under different osmotic conditions. Lowering the osmolarity to 262 mosM (83% of control) resulted in a rapid cell swelling which was followed by regulatory volume decrease (RVD). RVD was completely inhibited by furosemide (1 mM), an inhibitor of Cl-/cation co-transport. The hypotonic medium (262 mosM) induced a rapid and strong increase in 86Rb+ efflux from beta-cell-rich mouse pancreatic islets and the furosemide-sensitive portion of the efflux was significantly increased. A slightly less hypotonic medium (285 mosM, 90% of control) induced only cell swelling and no RVD. With this medium only a marginal increase in 86Rb+ efflux was observed. Increasing the osmolarity by adding 50 mM NaCl (final osmolarity: 417 mosM, 132% of control) induced a rapid cell shrinkage but no regulatory volume increase (RVI). When the osmolarity was increased from a slightly hypotonic medium (262 mosM) to an isotonic medium (317 mosM) an initial cell shrinkage was followed by RVI. This RVI was inhibited by 1 mM furosemide. The data suggest that RVD as well as RVI in the beta-cells are mediated by loop diuretic-sensitive cotransport of chloride and cations and that these cells show a threshold for hypotonic stimulation of RVD.

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There are few reports on successful high-dose spironolactone treatment of refractory protein-losing enteropathy (PLE) caused by Fontan procedure. We report successful diuretics treatment with spironolactone and furosemide at standard dose, of refractory PLE in a patient with Noonan syndrome and repaired congenital heart disease. This is the first successful application of diuretics treatment in a patient with refractory PLE without Fontan procedure. This case illustrates that diuretics treatment can be the first-line treatment of PLE regardless of the causative physiology, and can be effective in refractory PLE with Noonan syndrome.

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We have previously shown that a single dose of nebulized furosemide improves tidal volume and pulmonary compliance for up to a 2-hour study period. This study is undertaken in order to find out (a) whether increasing the dose of nebulized furosemide from 1 to 2 mg/kg of body weight will further improve the pulmonary mechanics in premature infants with evolving chronic lung disease and (b) whether the effects of a single dose of nebulized furosemide last beyond 2 hours.

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The authors report 13 cases of idiopathic subvalvular left ventricular aneurysm (ISVLVA), observed over a 7-year period in a total of 29,617 patients (0.04%). They describe the clinical features, results of complementary investigations and clinical course of this disease. The diagnosis was based on angiographic and anatomical findings in 4 cases and on echocardiographic findings in 10 cases. This series consisted of 10 females and 3 males with a mean age of 37.3 +/- 2.1 years (range: 9 to 72 years). Clinical signs consisted of palpitations in 2 cases, angina pectoris in 4 cases, heart failure in 9 cases, and systolic murmur of mitral incompetence in 13 cases. Chest x-rays showed vaulting of the left ventricle in 8 cases (61.5%). ECG showed sinus rhythm in 11 cases, atrial fibrillation in 2 cases, ventricular tachycardia in 1 case and junctional tachycardia in 1 case. The erythrocyte sedimentation rate was raised in 10 cases (76.9%). Complementary examinations revealed ISVLVA, which was often very large, calcified (7 cases), thrombosed (6 cases), situated on the posterolateral surface of the left ventricle, in a mitral subvalvular position (13 cases) and responsible for mitral incompetence (13 cases). The coronary arteries were normal in the 5 cases in which they were studied. No aetiology was found. Complications included death (1 case), heart failure (9 cases) and arrhythmias (3 cases). No systemic embolism was observed. Medical treatment (digoxin, furosemide, antiarrhythmics) was considered to be fairly effective, but insufficient to prevent episodes of heart failure and arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

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Hemorheologic changes 60 minutes after furosemide administration included increased PCV, plasma total protein concentration, whole blood viscosity, mean RBC volume, and RBC potassium concentration, and decreased serum potassium concentration, serum chloride concentration, and RBC chloride concentration. Furosemide treatment attenuated the exercise-associated changes in RBC size, serum sodium concentration, serum potassium concentration, RBC potassium and chloride concentrations, and RBC density; exacerbated exercise-associated increases in whole blood viscosity; and had no effect on RBC filterability.

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Forced diuresis coupled with parenteral hydration facilitates the acquisition of an artifact-free pelvic SPECT. Especially for clinical questions that focus on femoral heads and pubic bones, applying the aforementioned protocol may improve the diagnostic accuracy of pelvic bone SPECT.

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Enalaprilat (MK-422), an intravenously administered angiotensin-converting enzyme inhibitor, which is the parent compound of the oral angiotensin-converting enzyme inhibitor enalapril (MK-421), was studied in 11 patients with asymptomatic accelerated hypertension. Each patient received an initial intravenous dose of 1 mg, followed at one-hour intervals by enalaprilat 10 mg, furosemide 40 mg, and enalaprilat 40 mg. Six of 11 patients responded with a drop in mean arterial pressure greater than 15 mm Hg to diastolic levels below 110 mm Hg; there were four partial responders and one nonresponder. Pretreatment renins were not predictive of blood pressure response. No patient had any adverse reaction to the drug; there were no significant changes in posttreatment laboratory values. We conclude that enalaprilat is an effective, well-tolerated agent for the treatment of uncomplicated accelerated hypertension and its use does not imperil nonresponding uncomplicated patients.

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The addition of substrate in the form of lactate (L), but not glucose (G), increases the respiration of canine thick ascending limb (TAL) segments in a saturable (above 2 mM) fashion. More than 60% of this stimulation is ouabain-sensitive (1 mM ouabain) even if L and G transport are both sodium-insensitive processes in TAL. Thus L, but not G, specifically stimulates Na+ entry in TAL cells and its subsequent transport by the Na+,K(+)-ATPase. If chloride is substituted for by gluconate, no significant substrate-induced stimulation of ouabain-sensitive respiration is observed. SITS (4-acetamino-4'-isothiocyanostilbene-2,2'-disulfonic acid) also interferes with the L-induced stimulation of respiration. Thus L entry in TAL appears to be directly or indirectly coupled to the transepithelial flux of Cl-. Furosemide (F), but not amiloride, also inhibits this stimulation suggesting that the accelerated Na+ entry triggered by the application of L occurs through the F-sensitive carrier or that lactate transport is F-sensitive in TAL cells. In accord, F specifically impairs the metabolism of L (as compared to G). These data suggest that in intact TAL tubules both lactate uptake and oxidation are directly or indirectly influenced by the transcellular flux of NaCl. This organization may participate to maintain a stoichiometry between the transport of NaCl and the availability of L to support the energetic needs of TAL cells.

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

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Data were obtained from the REPOSI (REgistro POliterapie SIMI [Società Italiana di Medicina Interna]) registry, which enrolled 4035 patients in 2008 (n = 1332), 2010 (n = 1380), and 2012 (n = 1323). Multivariable logistic regression was performed to determine the risk factors independently associated with QT-prolonging drug use. QT-prolonging drugs were classified by the risk of Torsades de Pointes (TdP) (definite, possible, or conditional) according to the Arizona Center for Education and Research on Therapeutics (AzCERT) classification. Specific drug combinations were also assessed.

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We investigated possible renal protective and therapeutic effects of KW-3902 (8-(noradamantan-3-yl)-1,3-dipropylxanthine), a novel and potent adenosine A1-receptor antagonist, on cisplatin-induced acute renal failure (ARF). ARF was induced in rats by a single injection of cisplatin-induced acute renal failure (ARF). ARF was induced in rats by a single injection of cisplatin (5 mg/kg, i.v.). Prophylactic treatment with KW-3902 (0.01-1 mg/kg, p.o., twice a day) significantly attenuated the increases of serum creatinine (S-CRE) and urea nitrogen (S-UN) induced by cisplatin. On the other hand, neither furosemide nor trichlormethiazide showed any ameliorating effects against the cisplatin-induced ARF. In the clearance study, the cisplatin-treatment induced marked decreases of glomerular filtration rate (GFR), renal plasma flow (RPF), and reabsorptions of water, sodium and potassium at tubular sites, in comparison with those in untreated normal rats. KW-3902 (0.1 mg/kg, p.o., twice a day) significantly improved these deteriorated glomerular and tubular functions. In the rats with established cisplatin-induced ARF, KW-3902 ameliorated the cisplatin-induced reductions of GFR, RPF, and reabsorptions of water, sodium and potassium at tubular sites. These results suggest that activation of adenosine A1-receptors is involved in the pathogenesis of cisplatin-induced ARF. The adenosine A1-receptor antagonist may be useful for the treatment of cisplatin-induced ARF.

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In 48 patients (p) with hypertensive crisis (HC) the effect of nifedipine (N) sublingual 10-20 mg alone (group I, n = 19, mean control AH +/- SD 232 +/- 15.3/132.5 +/- 4.9 mmHg) or associated with furosemide and clonidine (group II, n = 29, AT 249 +/- 21/131.8 +/- 13.6 mmHg). In both groups the AT fell significantly starting five minutes after the administration of N (except diastolic AT in group II); the values measured at 45 min. being 177 +/- 32/105.4 +/- 13 mmHg in group I and 164.6 +/- 44.4/100.1 +/- 16.3 mmHg in group II (the mean proportional difference at 45 min. for systolic AT was 24.6 +/- 11.4% in group I and 28.7 +/- 12.2% in group II; for diastolic AT 20.5 +/- 9.4% in group I, and 27 +/- 12.2% for group II). The good clinical results consisted of lowering of the AT values below critical levels and clinical improvement in 42 p (87.5%). Tolerance to N was good, in a single case was hypotension associated with fainting, both being promptly treated by simple means. CONCLUSIONS. 1. N administered sublingual, 10-20 mg, alone or associated with furosemide has in most patients a rapid hypotensive effect, lowering AT below critical limits within 45 min; 2. the drug is readily administered and without the risk of side effects and can be used in the field in the emergency treatment of hypertension.

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We have previously found that the administration-time-dependent change in the effects of furosemide, a loop diuretic agent, is observed in normal rats. The present study was undertaken to examine whether an alteration in this phenomenon occurs in rats with DOCA-saline hypertension. Unilateral nephrectomized rats were divided into three groups. The first group (DOCA-saline) received a 50 mg DOCA tablet intraperitoneally and drank 1% NaCl solution. The other two groups were given sham operations. A 1% NaCl solution was given as drinking water to the second group (control-saline), while tap water was given to the third group (control-water). Furosemide (30 mg/kg) was given orally to each group at 12 a.m. or 12 p.m. Urine was collected for 8 hours after the agent, and urinary excretion of sodium and furosemide were determined. Urine volume and urinary excretion of sodium and furosemide following the agent were significantly greater at 12 a.m. than at 12 p.m. in the control-water and control-saline groups. However, the administration-time-dependent changes in these parameters disappeared in the DOCA-saline rats. These results suggest that the mode of the administration-time-dependent changes in the effects of furosemide is altered in the DOCA-saline hypertensive rats.

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Of the 18 identified interventions, 15 reduced mortality and 3 increased mortality. Perioperative hemodynamic optimization, albumin in cirrhotic patients, terlipressin for hepatorenal syndrome type 1, human immunoglobulin, peri-angiography hemofiltration, fenoldopam, plasma exchange in multiple-myeloma-associated AKI, increased intensity of renal replacement therapy (RRT), CVVH in severely burned patients, vasopressin in septic shock, furosemide by continuous infusion, citrate in continuous RRT, N-acetylcysteine, continuous and early RRT might reduce mortality in critically ill patients with or at risk for AKI; positive fluid balance, hydroxyethyl starch and loop diuretics might increase mortality in critically ill patients with or at risk for AKI. Web-based opinion differed buy lasix from consensus opinion for 30% of interventions and self-reported practice for 3 interventions.

lasix 10mg tablet 2016-06-18

We classified 518 children into 9 etiology groups: intrahepatic disease (IH) (105), hepatic vein outflow obstruction (HVOO) (45), congestive heart disease (CH) (33), nephrotic syndrome (NS) (36), pancreatitis (26), inflammatory and infectious diseases (77), malignancy (49), idiopathic (71), and miscellaneous (76). IH and CH were predominant in the younger age group (0-5 years) versus HVOO, pancreatitis, and malignancy in the older age group (13-21 years) (P < 0.001). The prevalence of ascites increased over time from 1983 to 2006 and declined thereafter. Ascites grade 1 was more common than ascites grades 2 and 3 in all the groups (P =  buy lasix 0.048). IH and NS were more likely to have ascites grade 2 and 3 (P = 0.02). Although spironolactone was more frequently used in the IH group versus other etiologies, furosemide was used more frequently in NS and CH versus other etiologies (P < 0.001).

lasix 200 mg 2015-06-21

We report a case buy lasix of acute respiratory distress after upper airway obstruction following routine palatoplasty in an otherwise healthy 6-year-old boy. We believe that extreme variation of intrathoracal pressure was the basis of the development of the acute respiratory distress. We recommend after palatoplasty a more than careful postoperative clinical observation to detect and treat postoperative obstruction and hypoxemia.

lasix 3 mg 2016-07-19

Since similar series report a mortality rate of 33-79%, it is suggested that early peritoneal dialysis may have positively influenced the final survival buy lasix rate.

lasix dose 2016-05-21

To measure the frequency dynamics of the vestibular evoked myogenic potential in patients with endolymphatic buy lasix hydrops.

lasix 8 mg 2016-05-11

Renal BOLD MRI, primarily at 1.5 T, has been shown to be useful for monitoring changes in medullary oxygenation status. We performed the present studies on buy lasix a 3.0 T scanner using a multiple gradient-echo (mGRE) sequence with a multicoil array to acquire 16 T2*-weighted images within a single breath-hold. Data were obtained before and after administration of furosemide (20 mg iv).

lasix dosage elderly 2015-07-08

Torasemide has been reported to reduce myocardial buy lasix fibrosis in patients with chronic heart failure (HF).

lasix 40mg tab 2016-05-05

CLC-K blockers may represent a new buy lasix class of drugs for the treatment of conditions associated with expanded extracellular volume, with a hopeful high therapeutic potential for hypertensive patients carrying ClC-K gain-of-function polymorphisms.

lasix pill 2015-12-30

Breathlessness is a common and difficult symptom to treat in patients with cancer. Case reports suggest that nebulised buy lasix furosemide can relieve breathlessness in such patients but few data are available.

lasix recommended dosage 2016-02-19

The outcome for the fetus with hydrops fetalis secondary to complete congenital heart block is almost uniformly buy lasix poor. Transplacental fetal therapy with inotropic drugs may be unreliable in the hydropic fetus. We describe our experience of direct fetal therapy with digoxin and furosemide in three cases.

lasix buy online 2017-06-01

Suspected alpha lipoic acid (ALA) toxicity was diagnosed based on buy lasix clinical history and compatible laboratory findings in 2 dogs. Case 1 was presented within 10 hours of ALA ingestion, with initial behavioral changes likely due to hypoglycemia. During the course of hospitalization, hypoglycemia persisted and evidence of acute hepatic insult developed. With aggressive supportive care (including IV fluids with dextrose supplementation, hepatoprotective medications, and a plasma transfusion), he made a full recovery. Case 2 was presented approximately 60 hours after ALA ingestion, and was found to be in oliguric renal failure. She was treated with IV fluids, gastroprotective medications, and furosemide, but her condition deteriorated and she was ultimately euthanized within 16 hours of admission to the hospital.

lasix 20mg cost 2016-03-14

We have previously reported a high prevalence of endemic renal tubular acidosis (EnRTA) in the northeast of Thailand, and our subsequent studies provided evidence that K deficiency exists in the same region. Since tubulointerstitial damage is associated with K deficiency, we postulate that this might be implicated in the pathogenesis of EnRTA and, if so, that a spectrum of buy lasix tubulointerstitial abnormalities can be anticipated. In this study we evaluated renal acidification ability in 4 patients and in 11 of their relatives. We used a 3-day acid load (NH4Cl 0.1 g/kg/day) followed by 20 mg oral furosemide and monitored the maximal renal concentrating ability using water deprivation and intranasal 1-deamino-D-arginine vasopressin. The results showed that the subjects could be divided into three groups; normal relatives of the patients, those with suspected renal tubular acidosis, and patients with overt EnRTA who had chronic metabolic acidosis and a low rate of excretion of NH4+. The rate of excretion of K was very low (20 +/- 4 mmol/day) in patients with EnRTA and in their relatives with suspected EnRTA. The transtubular K concentration gradient was also very low in their relatives, especially in patients with suspected EnRTA (2.8 +/- 0.2). With a 3-day NH4Cl load, the rate of excretion of NH4+ was very low in patients with EnRTA (32 +/- 9 mmol/day), and the relatives with suspected EnRTA also had a decreased capacity to excrete NH+4 (50 +/- 14 mmol/day). In contrast, the normal relatives excreted 92 +/- 12 mmol of NH+4/day. The patients with EnRTA could lower their urine pH to less than 5.5 after the acid loading (6.2 +/- 0.3). After furosemide (20 mg), the NH4+ excretion in the patients with EnRTA was lower than in the normal relatives. Moreover, the minimum urine pH in patients with EnRTA did not fall (6.1 +/- 0.2), but there was a fall to 4.8 +/- 0.1 in the patients with suspected EnRTA after furosemide treatment. In conclusion, there was a spectrum of tubulointerstitial abnormalities ranging from suspected to overt distal RTA in a geographic area known to have a high prevalence of K deficiency. K deficiency might be the important pathogenetic factor of EnRTA in the northeast of Thailand.

lasix 10 mg 2016-07-01

γ-Aminobutyric acid (GABA)ergic transmission plays an important role in the initiation of epileptic activity and the generation of ictal discharges. The functional alterations in the epileptiform hippocampus critically buy lasix depend on GABAergic mechanisms and cation-chloride cotransporters.

lasix medication 2017-06-07

Rapid recovery from acoustic trauma was temporally correlated with urodynamic and cardiovascular reactions from ingesting food containing sulfite preservative, a substance to which the individual was allergic. Factors that buy lasix may have contributed to recovery of function include massive diuresis, increased heart rate, release of biochemical mediators, mediator-induced vasodilatation, and changes in vascular or cell membrane permeability. Establishing relationships that lead to recovery of function from acoustic trauma may facilitate research and aid in the development of new treatment options for this condition.

lasix 160 mg 2017-02-23

Dilated cardiomyopathy (DCM) refers to a group of conditions of diverse etiology in which both ventricles are enlarged with reduced contractility. Certain correctable conditions associated with ventricular dysfunction can masquerade as DCM. Most of them can be identified with relatively inexpensive and readily available tests. A typical diagnostic work-up for a child with DCM also includes a number of investigations to identify the underlying cause, some of which are expensive and sophisticated. The average center in the developing world often does not have the facilities to carry out these investigations. The results of many of these investigations typically do not translate into a specific management strategy that makes a difference to prognosis. A significant number of children with DCM will eventually develop end-stage heart failure Baclofen Lioresal Dosage that requires cardiac transplantation with or without bridging procedures. This is an unrealistic option for the developing world. The management strategy of childhood DCM in the developing world needs to be tailored to the resources available with in a manner such that the overall prognosis is not substantially affected.

lasix 40mg tablet 2016-08-19

Myocardial infarction was Levitra Tab 20mg produced by coronary artery ligation in spontaneously hypertensive rats. The rats were randomly assigned to receive either ramipril (1 mg/kg/day), furosemide (4 mg/kg/day), or combination therapy for 6 weeks, commencing 2 weeks after infarction.

lasix reviews 2017-03-31

Insulin resistance is associated with hypertension by mechanisms likely involving the kidney. To determine how the major apical sodium transporter of the thick ascending limb, the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2) is regulated by high-fat feeding, we treated young male, Fischer 344 X Brown Norway (F344BN) rats for 8 wk with diets containing either normal (NF, 4%) or high (HF, 36%) fat, by weight, primarily as lard. HF-fed rats had impaired glucose tolerance, increased urine excretion of 8-isoprostane (a marker of oxidative stress), increased protein levels for NKCC2 (50-125%) and the renal outer medullary potassium channel (106%), as well as increased natriuretic response to furosemide (20-40%). To test the role of oxidative stress in this response, in study 2, rats were fed the NF or HF diet plus plain drinking water, or water containing N(G)-nitro-l-arginine methyl ester (l-NAME), a nitric oxide synthase inhibitor (100 mg/l), or tempol, a superoxide dismutase mimetic (1 mmol/l). The combination of tempol with HF nullified the increase in medullary NKCC2, while l-NAME with HF led to the highest expression of medullary NKCC2 (to 498% of NF mean). However, neither of these drugs dramatically affected the elevated natriuretic response to furosemide with HF. Finally, l-NAME led to a marked increase in blood pressure (measured by radiotelemetry), which was significantly enhanced Parlodel Ovulation Drug with HF. Mean arterial blood pressure at 7 wk was as follows (mmHg): NF, 100 +/- 2; NF plus l-NAME, 122 +/- 3; and HF plus l-NAME, 131 +/- 2. Overall, HF feeding increased the abundance of NKCC2. Inappropriately high sodium reabsorption in the thick ascending limb via NKCC2 may contribute to hypertension with insulin resistance.

lasix oral dosage 2015-02-07

Potassium (using 86Rb+ as a tracer), amino acid and taurine fluxes were measured in horse red blood cells (RBCs). No volume-sensitive component of alanine and glycine transport was observed, and although volume-sensitive taurine fluxes were observed in most animals, their absolute magnitudes were small. K+ fluxes, however, were shown to be particularly volume sensitive; they were stimulated by cell swelling and inhibited by cell shrinkage. Sizeable fluxes were present at normal cell volumes. The volume-sensitive K+ flux was Cl- dependent and was Singulair Pill abolished by Cl- replacement with methylsulphate. The Cl(-)-dependent K+ fluxes in horse red blood cells were stimulated by lowering in external pH to 6.9 and by treatment with the sulphydryl-reacting agent, N-ethylmaleimide. They were inhibited by the potent K(+)-Cl- co-transport inhibitor, DIOA, ([(dihydroindenyl)oxy]alkanoic acid) but were insensitive to the Na(+)-K(+)-Cl- co-transport inhibitors, frusemide and bumetanide. A Cl- channel inhibitor, 5-nitro-2-(phenylpropyl-amino)-benzoate (NPPB), produced partial inhibition. These results suggest that regulatory volume decrease in horse red blood cells is achieved predominantly by volume-sensitive K+ efflux mediated via a K(+)-Cl- co-transport system with similar properties to those observed in the red blood cells of other species. The significance of these findings and their rheological consequences are discussed.

lasix 70 mg 2017-10-07

Involvement of AVP in several pathological states is now established and specific modulation of the different AVP receptor subtypes (V1a, V1b and V2) offers new clinical perspectives for treating major diseases. Recent years have marked a turning point with the design and the use of the first nonpeptide vasopressin receptor antagonists expressing various selectively profile. In that field, we report here the characterization of SR 121463A a highly selective, orally-active antagonist of vasopressin V2 receptors in several models in vitro and in vivo. This compound displayed competitive nanomolar affinity for V2 receptors in various species including man and exhibited a highly selective AVP V2 profile. In vitro, SR 121463A potently antagonized AVP-stimulated adenylyl cyclase activity in human kidney preparations (Ki = 0.26 +/- 0.04 nM) without any intrinsic agonistic effect. In normally-hydrated rats, SR 121463A induced dose-dependent powerful and long-lasting aquaresis after intravenous (0.003 to 0.3 mg/kg) or oral (0.03 to 10 mg/kg) administration. The action of SR 121463A is purely aquaretic with no changes in urine Na+ and K+ excretions unlike that of known diuretic agents such as furosemide or hydrochlorothiazide. In vasopressin-deficient Brattleboro rats, SR 121463A is devoid of any V2 antidiuretic agonist properties. In addition, this compound potently antagonized DDAVP extrarenal V2 effects on hemostasis factor release (FVIII, vW and t-PA) in dogs (ID50 approximately 10 micrograms/kg i.v.). Thus, SR 121463A is the most potent and Seroquel 6 Mg selective, orally-active V2 antagonist yet described. It is a useful ligand for exploring V2 receptors and the therapeutical usefulness of pure V2 aquaretic agents in several water-retaining diseases and congestive heart failure.

lasix order 2015-07-07

Until now the effect of thallium (Tl) on renal function has not been investigated systematically. Therefore, the dose (5, 10, 15, 20 mg Tl2SO4/kg body wt., intraperitoneally) and time-dependence of renal damage was investigated in diuresis experiments on conscious rats. Morphology was evaluated after perfusion fixation in situ. Morphologic changes were localized in the thick ascending limb of the loop of Henle, mostly expressed at the 2nd day after Tl administration, which were completely normalized again at the 10th day. Other parameters such as Tl concentration, changes in water content and Luvox Typical Dosage the activity of Na+/K(+)-ATPase as well as the diuretic effect of furosemide confirmed the Tl effect to be localized in the renal medulla. One single Tl administration is followed by a decrease in glomerular filtration rate (GFR) and urine volume and an increase of proteinuria. Electrolyte excretion was only slightly changed. All changes were reversible within the 10-day investigation period.

lasix dosage racehorses 2017-06-30

The effect of furosemide on insulin release, glucose oxidation, 36Cl- fluxes, and 45Ca2+ uptake was studied in isolated, beta-cell-rich pancreatic islets from ob/ob mice. Low concentrations of furosemide (0.01-0.1 mM) reduced the glucose-induced insulin release, whereas high doses (1-10 mM) increased basal and glucose-induced release. Furosemide at concentrations that reduced glucose-induced insulin release (0.01-0.1 mM) did not affect the islet production of 14CO2 from D-[U-14C]glucose. The influx rate and equilibrium content of 36Cl- were reduced by furosemide, whereas the basal and glucose-stimulated 36Cl- efflux rates were unaffected. The glucose-induced (10 mM) uptake of 45Ca2+ was inhibited by furosemide. It is suggested that the diabetogenic action of Lexapro 7 Mg furosemide may be due, at least in part, to direct inhibition of insulin release from the pancreatic beta-cells. This may be caused primarily by inhibition of an inwardly directed Cl- pump, leading to a reduced transmembrane electrochemical gradient for chloride in the beta-cells. This reduced gradient in combination with unaltered Cl- permeability may lead to decreased total outward Cl- transport, a factor associated with stimulated calcium uptake and insulin release.

lasix cost 2016-06-23

Rundown of ionic gradients is a central feature of white matter anoxic injury; however, little is known about the contribution of anions such as Cl-. We used the in vitro rat optic nerve to study the role of aberrant Cl- transport in anoxia/ischemia. After 30 min of anoxia (NaN3, 2 mm), axonal membrane potential (V(m)) decreased to 42 +/- 11% of control and to 73 +/- 11% in the presence of tetrodotoxin (TTX) (1 microm). TTX + 4,4'-diisothiocyanatostilbene-2,2' disulfonic acid disodium salt (500 microm), a broad spectrum anion transport blocker, abolished anoxic Valtrex Maximum Dosage depolarization (95 +/- 8%). Inhibition of the K-Cl cotransporter (KCC) (furosemide 100 microm) together with TTX was also more effective than TTX alone (84 +/- 14%). The compound action potential (CAP) area recovered to 26 +/- 6% of control after 1 hr anoxia. KCC blockade (10 microm furosemide) improved outcome (40 +/- 4%), and TTX (100 nm) was even more effective (74 +/- 12%). In contrast, the Cl- channel blocker niflumic acid (50 microm) worsened injury (6 +/- 1%). Coapplication of TTX (100 nm) + furosemide (10 microm) was more effective than either agent alone (91 +/- 9%). Furosemide was also very effective at normalizing the shape of the CAPs. The KCC3a isoform was localized to astrocytes. KCC3 and weaker KCC3a was detected in myelin of larger axons. KCC2 was seen in oligodendrocytes and within axon cylinders. Cl- gradients contribute to resting optic nerve membrane potential, and transporter and channel-mediated Cl- fluxes during anoxia contribute to injury, possibly because of cellular volume changes and disruption of axo-glial integrity, leading to propagation failure and distortion of fiber conduction velocities.

lasix 40 mg 2016-09-27

Partial displacement of cerebellar [(3)H]EBOB binding by nanomolar HBAO was attenuated by 0.1 mM furosemide, an antagonist of alpha(6) and beta(2-3) subunit-containing GABA(A) receptors. Displacement curves of HBAO were reshaped by 30 nM GABA and shifted to the right. However, the micromolar potency of full Protonix Oral Dosage displacement by allopregnanolone was not affected by 0.1 mM furosemide or 30 nM GABA. The nanomolar, but not the micromolar phase of displacement of [(3)H]EBOB binding by GABA was attenuated by 100 nM HBAO. Submicromolar HBAO did not affect [(3)H]EBOB binding to cortical and hippocampal GABA(A) receptors. HBAO up to 1 microM did not affect chloride currents elicited by 0.3-10 microM GABA, while it abolished potentiation by 1 microM allopregnanolone with nanomolar potency in cerebellar but not in cortical cells. Furosemide attenuated cerebellar inhibition by 100 nM HBAO.

lasix 240 mg 2015-02-02

Mg2+-extrusion from Mg2+-loaded neurons of the leech, Hirudo medicinalis, is mediated mainly by Na+/Mg2+ antiport. However, in a number of leech neurons, Mg2+ is extruded in the nominal absence of extracellular Na+, indicating the existence of an additional, Na+-independent Mg2+ transport mechanism. This mechanism was investigated using electrophysiological and microfluorimetrical techniques. The rate of Na+-independent Mg2+ extrusion from Mg2+-loaded leech neurons was found to be independent of extracellular Ca2+, K+, NO3-, HCO3-, SO4(2-), HPO4(2-), and of intra- and extracellular pH. Na+-independent Mg2+ extrusion was not inhibited by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), furosemide, ouabain, vanadate, iodoacetate, 4-amino-hippurate, or alpha-cyano-4-hydroxycinnamate and was not influenced by changes in the membrane potential in voltage-clamp experiments. Na+-independent Mg2+ extrusion was, however, inhibited by the application of 2 mM probenecid, a blocker of organic anion transporters, suggesting that Mg2+ might be co-transported with organic anions. Extracellularly, of all organic anions tested (malate, citrate, lactate, alpha-ketoglutarate, and 4-amino-hippurate) only high, but physiological, concentrations of malate (30 Diovan Starting Dose mM) had a significant inhibitory effect on Na+-independent Mg2+ extrusion. Intracellularly, iontophoretically injected malate, citrate, or fura-2, but not Cl-, alpha-ketoglutarate, glutamate, succinate, or urate, were stimulating Na+-independent Mg2+ extrusion from those neurons that initially did not extrude Mg2+ in Na+-free solutions. Our data indicate that Mg2+ is co-transported with organic anions, preferably with malate, the predominant extracellular anion in the leech. The proposed model implies that, under experimental conditions, malate drives Mg2+ extrusion, whereas under physiological conditions, malate is actively taken up, driven by Mg2+, so that malate can be metabolized.

lasix generic 2015-12-05

Both groups 1 and 2 had significantly slower rates of decline in glomerular filtration rate compared with group 3. No significant differences were observed in renal hemodynamics between groups 1 and 2 at 18 months. Group 3 had the worst metabolic, lipid, and side-effect profile of any group. Reductions in albuminuria were not different between groups 1 and 2, but both were significantly reduced compared with group 3.

lasix fluid pill 2016-05-09

The response to incremental doses of oral labetalol in 16 patients with hypertensive urgencies is presented. After inadequate blood pressure control with 20 mg of intravenous furosemide, each patient received a 300 mg oral dose of labetalol. Subsequent oral doses of labetalol, 100 mg, were administered at 2-hour intervals, if the diastolic blood pressure remained greater than 100 mm Hg. The maximum dose of labetalol per patient was 500 mg. Five patients required only the initial 300 mg dose of labetalol. Two patients required further therapy for satisfactory blood pressure control. Mean arterial pressure fell from 156 +/- 12 mm Hg to 123 +/- 14 mm Hg.

lasix 80mg tab 2015-02-28

Hysteroscopical myomectomy has recently become popular in Japan. We present two patients who developed water intoxication and air embolism during surgery. [Case 1] Hysteroscopical myomectomy was performed under general anesthesia in a 37-yr-old woman (ASA I). Three hours after the start of the surgery, the patient's serum sodium concentration dropped to 118 mEq.l-1. She was treated with furosemide and recovered without sequelae. [Case 2] A 39-yr-old woman (ASA I) was scheduled to have hysteroscopical myomectomy under spinal and epidural anesthesia. Forty-five minutes after the start of the surgery, the patient complained of severe back pain, her blood pressure decreasing to 40 mmHg, SpO2 decreased to 80%, and ECG showed atrial fibrillation. After administration of ephedrine 5 mg, she recovered within 20 min. No abnormality was observed in echocardiogram, although some negative spots were detectable in a lung scintigraphy. She was discharged without sequelae. The hysteroscopical procedure is considered a non-invasive surgery, but the cases presented here emphasize the necessity for close attention to complications, especially pulmonary embolism.

lasix normal dosage 2016-12-28

The present study investigated the involvement of capsaicin-sensitive sensory neurons on salt intake control in the rat, following capsaicin neonatal treatment. Capsaicin did not affect salt appetite induced by intramuscular injection of deoxycorticosterone enantate, or by intracranial injection of renin. Moreover, it did not alter salt preference of rats given access to a variety of NaCl concentrations, or the need-free salt intake of multidepleted male rats. On the other hand, in response to furosemide-induced sodium depletion, the salt intake of capsaicin-treated rats was lower than that of controls. However, furosemide-induced Na+ excretion of capsaicin-treated rats proved to be lower than that of controls, thus suggesting that difference in salt intake might be secondary to lower sensitivity of capsaicin-treated rats to the natriuretic action of furosemide. Salt intake is known to be influenced by sensory information from the oral cavity, from the liver and from the intravascular compartment. The absence of effect of capsaicin neonatal treatment suggests that sensory fibers relevant to salt intake control may not be capsaicin sensitive. On the other hand, our findings indicate that capsaicin treatment alters the renal response to furosemide and stimulate further studies on the effects of capsaicin on renal function.