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Lasix

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.

Description

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.

Dosage

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.

Overdose

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.

Storage

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.

Contraindications

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 drug class

Of 52 cases with 56 affected renal units having symptoms and signs suggestive of Ureteropelvic Junction Obstruction (UPJO) evaluated by conventional (F + 15) diuretic renography where frusemide is given 15 minutes post-injection of radiopharmaceutical m99TC.DTPA.F + 15, twelve (21%) showed a good clearance (group A), 16 (28%) showed partial (group B) and 28 (50%) a poor clearance pattern (group C) indicating a definite obstruction. A high flow (F-15) diuretic renography where frusemide is given 15 minutes prior to the radiopharmaceutical m99TC.DTPA, was done in 23 cases with 27 affected renal units. Eleven renal units showed a good clearance (group A). Of these, 7 (64%) showed a persistent good clearance, 3 (27%) converted to poor clearance and 1 (9%) to partial clearance pattern. Of 8 renal units in group B, 5 (63%) converted to poor clearance and two (25%) to good clearance on F-15 and one remained unchanged. All renal units which presented as poor clearance (group C) on conventional (F + 15) diuretic renography remained unchanged on high flow (F-15) diuretic renography. In majority of cases conventional (F + 15) renography gave a reliable assessment of the upper tract drainage, however, since equivocal group was resolved by the F-15 and the intermittent obstruction group was definitely diagnosed, high flow (F-15) diuretic renography was more conclusive in assessment as compared to F + 15.

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It was shown in chronic rat experiments that multiple microinjections of furosemide into the rostral region of the neostriatum facilitated avoidance conditioning in a shuttle box and prevented from GABA-induced deviant freezing, but did not abolish the choreic hyperkinesis produced by picrotoxine (GABA-A receptors antagonist) intrastriatal microinjections. Simultaneous microinjections of furosemide and picrotoxine into the neostriatum increased differences in parameters of picrotoxine-induced hyperkinesis between rat groups capable and incapable (extinct reflex) for conditioned avoidance. These findings point to a certain correlation between the intensity of hyperkinesis, capability for acquisition and realization of avoidance conditioning, and activity of neostriatal neurotransmitter systems involved in neuronal homeostasis. The findings suggest an involvement of neostriatal GABAergic system in conditioning and organization of free locomotor behavioral acts.

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Myo-inositol is a major compatible osmolyte in the renal medulla and is accumulated in cells under hypertonic conditions by uptake via a Na+/myo-inositol cotransporter (SMIT). SMIT is regulated by extracellular osmolarity at the transcription level. We investigated localization of SMIT in rat kidney by immunohistochemical staining using an anti-SMIT-antibody raised against a synthetic peptide corresponding to part of SMIT and by in situ hybridization. SMIT protein localized predominantly to the basolateral membranes of cells of the thick ascending limb of Henle (TAL) and inner medullary collecting duct (IMCD). Macula densa (MD) cells, identified as the Tamm-Horsfall-protein (THP)-unreactive cells surrounded by THP-reactive TAL cells, also stained for anti-SMIT. In situ hybridization yielded the intense SMIT signals in the TAL and IMCD and also in the juxtaglomerular (JG) region. Prior loading of the animal with a high concentration of NaCl rapidly induced SMIT mRNA; furosemide down-regulated it. The high level of SMIT expression suggests that MD cells are exposed to hypertonicity at the basolateral surface. Because SMIT expression seemed to be proportional to the magnitude of NaCl reabsorption, it may be a good marker for examination of the tubuloglomerular feedback mechanism in vivo.

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A 13-year-old llama was examined because of lethargy, inappetence, and syncope.

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We assigned heart transplant recipients 18 years of age or older who were oliguric (urine output < 400 ml/day); had volume overload and estimated glomerular filtration rate <60 ml/min/1.73 m(2) of body surface area calculated with the use of the Modification of Diet in Renal Disease equation, to designed initiation of intervention. We followed 30 patients for up to 30 days. The primary outcome was estimated glomerular filtration rate status after intervention.

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This study was designed to assess: (1) whether furosemide modifies the incidence of failure to close a symptomatic patent ductus arteriosus (PDA) in response to indomethacin in premature infants, (2) whether furosemide decreases renal and hydromineral side effects of indomethacin, and (3) whether the effects of furosemide on renal function depend on initial extracellular volume [assessed by blood urea nitrogen (BUN)/creatinine ratio]. We did a systematic review and meta-analysis of all published controlled trials assessing either ductal closure or renal function after randomized allocation to treatment with indomethacin and furosemide versus indomethacin alone. All of the three studies meeting entry criteria were small and had methodological limitations. The number of patients was too small to rule out a 10% risk increase in failure of ductal closure. After the first dose of indomethacin, patients receiving furosemide had higher urine output, fractional excretion of sodium, and osmolar clearance than controls. Among patients with initial BUN/creatinine ratio <20, those on furosemide had a higher glomerular filtration rate (GFR) than controls. Among patients with initial BUN/creatinine of 20-30, those on furosemide had a lower GFR than controls. Thus, dehydration appears to be a contraindication for furosemide administration in premature infants treated with indomethacin for symptomatic PDA. The risk-benefit ratio of administering furosemide in well-hydrated patients treated with indomethacin for symptomatic PDA could only be assessed by a large randomized clinical trial.

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Laparoscopic partial nephrectomy (LPN) has not received widespread clinical application because of its technical challenge. Bovine serum albumin glutaraldehyde (BSAG) is a hemostatic agent that is independent of the clotting cascade. We evaluated the use of BSAG as the sole agent for parenchymal and collecting system closure during LPN in a survival porcine model.

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A 61-year-old man suffering from histologically confirmed amyloidosis associated with coagulation disturbances presented with exercise induced shortness of breath and symptoms of cardiac asthma after four cycles of chemotherapy with melphalan and prednisolone. As a result, treatment with digitoxin was initiated. In addition furosemide and an oral nitrate were administered.

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To determine whether gamma-aminobutyric acid (GABA) affects the contractile properties of airway smooth muscle and, if so, what the mechanism of action is, the authors studied guinea pig tracheal rings under isometric conditions in vitro. GABA and related substances, baclofen and muscimol, had no effect on the resting tension but reversibly depressed contractions induced by electrical field stimulation in a dose-dependent fashion, IC50 values (mean +/- S.E.) being 5.6 +/- 1.4 X 10(-6) M, 6.8 +/- 0.9 X 10(-6) M and 8.5 +/- 1.5 X 10(-5) M, respectively. In contrast, GABA did not alter the response to exogenous acetylcholine or the nonadrenergic noncholinergic inhibitory component. Pretreatment of tissues with bicuculline antagonized the inhibitory effect of GABA as well as that of baclofen. This inhibitory effect was not modified by propranolol, phentolamine, hemicholinium-3 or naloxone, but it was blocked by the Cl channel blocker furosemide and by the substitution of external Cl. These results suggest that GABA decreases the contractile response of airway smooth muscle to cholinergic nerve stimulation by inhibiting the evoked release of acetylcholine and that this effect is exerted by activating Cl-dependent, bicuculline-sensitive GABA receptors.

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To investigate the effect of intravenous normal saline fluid load, with and without furosemide, upon the renal resistive index (RI) of obstructed and nonobstructed kidneys.

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The aim of the present study was to investigate the influence of the rate of delivery of frusemide to its site of action on the effect and efficiency of the drug.

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Rabbit tracheocytes were isolated by protease treatment and plated onto collagen-treated permeable supports at 1.3 x 10(6) cells/cm2. After 24 hr, cell layers were cultured either air-interfaced (AIC) on their apical surface or under conventional liquid covered conditions (LCC).

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To review medications that can affect serum calcium concentrations.

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The experiments were carried out on unanaesthetized dogs with exteriorized ureters. The left kidney was denervated. The function of the left and right kidneys was compared prior to and after furosemide administration, 0.2 mg/kg b. w. The function of the right intact kidney prior to and after left kidney denervation was also compared. The concentrations of sodium, potassium, chloride, calcium, magnesium, zinc, copper, urea, and creatinine in plasma and urine were determined. Denervation of the left kidney was followed by an increase of diuresis, calcium, and copper excretion from the denervated kidney. After furosemide administration the chloride excretion from the side of denervation was also observed to increase. The changes in the excretory function of the left kidney after denervation were not accompanied by changes in excretory function of right (intact) kidney. The excretory function of the intact kidney after denervation of contralateral kidney and furosemide administration did not differ from that prior to denervation and furosemide administration. In unanaesthetized dogs no changes in the excretory function of intact kidney were observed as a result of contralateral kidney denervation.

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Microcapsules with self-microemulsifying core were originated by the vibrating nozzle method. Alginate-pectin (A/P) ratio of the shell forming phase was optimized with regard to core phase retention and drug release kinetics from dried microcapsules. Well shaped microcapsules with high encapsulation efficiency were produced when an A/P composition of 25:75 was used. Microcapsules with higher pectin content exhibited faster drug release, which was additionally enhanced by the addition of sodium chloride to the shell phase.

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The existence of supranormal differential renal function in unilateral hydronephrosis remains controversial. While some authors consider it as fact, others believe that it is just a technical artifact. Within our department, chromium-51 ethylene diamine tetra-acetic acid (Cr-EDTA) renal clearance is systematically performed in conjunction with technetium-99m mercaptoacetyltriglycine (MAG3) renograms to derive an absolute single kidney glomerular filtration rate (SKGFR). Our data allows us to ascertain whether supranormal differential renal function in unilateral hydronephrosis might be due to hypofunction of the contralateral kidney. Children with marked unilateral hydronephrosis were selected from a large database of MAG3 diuretic(s) renograms. We excluded patients with posterior urethral valves, duplex anomalies, neurogenic bladder, solitary kidney, and those who underwent any previous urological surgery. We also excluded children who had an early furosemide injection (F0 procedure), selecting only those having received furosemide at the end of the renogram (F+20 test). Seventy-three patients (92 renograms) fulfilled these criteria. Differential renal function was calculated using the integral method. Hydronephrotic kidney with a relative uptake > or =55% was defined as supranormal. Six renograms (four patients) demonstrated supranormal relative function on the hydronephrotic side. However, the SKGFR of these kidneys was in all cases within the range of normal values, while the contralateral side demonstrated borderline low SKGFR. Increased relative function on the side of the hydronephrotic kidney is relatively infrequent. When it occurs, it may be related to a borderline hypofunction of the contralateral kidney.

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Four patients with thallium toxicity were treated with Prussian blue, 125 mg/kg/day. The diagnosis was made on clinical grounds and confirmed by detection of thallium in the urine. Electromyographic, evoked potentials and electroencephalographic studies confirmed quick clinical and electrophysiologic improvement of the patients.

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1. Adriamycin, a commonly used antineoplastic antibiotic, induces glomerular lesions in rats, resulting in persistent proteinuria and glomerulosclerosis. 2. The effect of urine volume on the progression of adriamycin-induced nephropathy was studied in 70 male Wistar rats (180-200 g) observed for 30 weeks and separated into 4 groups: healthy control group (HCG, N = 10) inoculated i.v. with 1 ml of saline, and nephrotic groups inoculated iv with a single dose of adriamycin of 3 mg/kg body weight. The nephrotic rats were separated into 3 groups (N = 20): nephrotic control group (NCG) receiving only adriamycin; dehydrated nephrotic group (DNG) water deprived for 36 h within each 48-h period, and furosemide nephrotic group (FNG) treated with 12 mg/dl furosemide, and 0.9 g/dl NaCl in the drinking water. 3. The 30-week survival rates of the DNG (100%) and HCG (100%) were significantly higher than those of the NCG (85%) and FNG (55%). 4. The proteinuria observed in the HCG (range, 7.38 +/- 0.7 to 13.6 +/- 1.27 mg/24 h) was significantly lower than that observed for all the nephrotic groups throughout the experiment. The DNG presented significantly less proteinuria (range, 42.71 +/- 6.83 to 140.10 +/- 19.22 mg/24 h) than the NCG (range, 35.32 +/- 7.64 to 250.00 +/- 25.91 mg/24 h) from week 10 on. There was no significant difference between the mean 24-h proteinuria of the NCG (range, 35.32 +/- 7.64 to 250.00 +/- 25.91 mg/24 h) and the FNG (range, 35.82 +/- 7.91 to 221.54 +/- 26.74). 5. The mean frequency of damaged glomeruli was 0.3% +/- 0.3 for HCG, 42% +/- 6% for CNG, 40.8% +/- 8% for DNG, and 47% +/- 14% for FNG. The median value of the tubulointerstitial lesion, evaluated by a semiquantitative method, was 0 in HCG, 10 in CNG, 8.5 in DNG and 9.5 in FNG (P < 0.05 for all groups compared to HCG). 6. The data indicate that reduction of urine volume has a protective effect on adriamycin-induced nephropathy.

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These results suggest the presence of an environmental etiology, rather than a genetic one, which is responsible for the development of hepatoblastoma in children of very low birthweight. Close monitoring of the children after being discharged from the neonatal intensive care unit is essential and a case-control study is necessary to identify risk factors for hepatoblastoma in children of very low birthweight.

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Ten consecutive patients with renal calculi underwent a modified four-detector multislice CTU with frusemide, abdominal compression and subsequent injection with contrast medium. After unenhanced CT of the abdomen, a high-resolution contrast-enhanced scan was taken through the kidneys in the pyelographic phase. Data were analysed using multiplanar reconstruction and three-dimensional (3D) reformatting.

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To report a case of presumed furosemide-associated bilateral angle-closure glaucoma.

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This was a retrospective cohort study of patients who received care from a large health system and had a primary hospital discharge diagnosis of HF between Jan 1, 2000 and June 30, 2008. Patients with preexisting end-stage renal disease were excluded. Daily creatinine (Cr) measurements, furosemide dosing (only loop diuretic on hospital formulary), and radiocontrast dye studies were collected using administrative data. Day-to-day changes in Cr and MDRD estimated glomerular filtration (eGFR) were calculated. The first Cr or eGFR value during hospitalization or in the emergency department was considered baseline. Generalized estimating equations were used to test the association furosemide exposure over previous 2 days to the daily change in Cr and eGFR. Covariates included undergoing radiocontrast study, age, race, gender, and baseline Cr or eGFR.

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As part of a prospective, randomised, nonblind study, we assessed the effects of torasemide and furosemide on readmission to hospital in 193 patients treated for CHF at a US urban public healthcare system. We also calculated total direct healthcare costs for the 2 drugs. The perspective of the analysis was that of the healthcare system. Healthcare charge and utilisation data, demographic information, and health status data were obtained from an electronic database containing data for all patients treated within the healthcare system.

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These experiments in isolated mouse cortical thick ascending limbs (cTALH) provide information about: the relative contributions of cellular and paracellular pathways to the transepithelial electrical conductance Ge (mS cm-2); the effects of (CO2 + HCO3-) on Ge; the ratio of net K+ secretion (JKnet) to net Cl- absorption (JClnet); and the K+ requirement for apical membrane furosemide-sensitive NaCl entry. The combination of luminal Ba++, zero K+ reduced Ge; at 5 mM luminal Ba++, the residual conductance was about 75% of the control Ge. The Ba++-insensitive Ge of 73.1 +/- 6.4 mS cm-2 was only slightly greater than the shunt conductance of 57 mS cm-2 computed from the sum of the dissipative bath to lumen fluxes of 22Na+ and 36Cl-. Moreover, luminal 5 mM Ba++, zero K+ had no effect on the Na+/Cl- permselectivity ratio of the paracellular pathway. Thus, Ba++ blockaded transcellular conductance by blocking apical membrane K+ channels. The combination of (CO2 + HCO3-) in external solutions increased Ge solely by augmenting the Ba++-sensitive, that is, transcellular, component of Ge. Finally, in paired experiments, the ratio JKnet/JClnet was 0.27 +/- 0.05; and both Ve, the spontaneous transepithelial voltage (mV), and the equivalent short circuit current Je (pEq sec-1 cm-2) were reduced dramatically by luminal K+ omission. Thus, apical membranes of the cTALH appear to contain a pathway for net K+ secretion, and apical membrane NaCl entry may involve co-transport with K+. Transcellular conductance contributes at least 25% to the total Ge, and the combination (CO2 + HCO3-) augments transcellular conductance.

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Hearing loss in neonatal intensive care unit (NICU) graduates range from 2% to 15% compared to 0.3% in full-term births, and the etiology of this discrepancy remains unknown. The majority of NICU admissions receive potentially ototoxic aminoglycoside therapy, such as gentamicin, for presumed sepsis. Endotoxemia and inflammation are associated with increased cochlear uptake of aminoglycosides and potentiated ototoxicity in mice. We tested the hypothesis that sepsis or systemic inflammatory response syndrome (SIRS) and intravenous gentamicin exposure increases the risk of hearing loss in NICU admissions.

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The median of age was 53+/-18 years old; 53% of the patients were women, and 34% were older than 65 years of age. Sixty-three percent of the patients received one prescription identified as potential D-DI, and 33.5% of these prescriptions were "major D-DIs". The most frequently pairs of drugs prescribed were: fluoroquinolones-hypoglycemics (20.5%), enoxaparin- nonsteroidal antiinflammatory drugs or anticoagulants (18.1%), furosemide- angiotensin converting enzyme inhibitors (ACE inhibitor) (12.2%), alopurinol-ACE inhibitor (9%), and spironolactone-ACE inhibitor (9%). Thirty-three percent of patients older than 65 years of age received a prescription including one potential D-DI. Gender and the number of drugs received were associated factors to the potential D-DI.

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What happened to each of the patients? On re-examination, the first person was in tears and unable to lie still, even after 20 mg of i.v. morphine sulfate. Capillary refill was still intact, but he had lost sensation to the dorsum of the foot and was unable to dorsiflex his toes. He had a marked elevation of compartment pressure, and his creatinine phosphokinase (see below) was twice normal. In the OR, a fasciotomy was performed. Some muscle necrosis had occurred. In the second patient, fluids were infused rapidly on arrival at the ED via the i.v. route. He was given morphine sulfate for pain control while we awaited laboratory results. After about 45 minutes, he produced dark red urine. His creatinine phosphokinase (diagnostic muscle enzyme test) was 190,000--nearly 1,000 times above normal. He also had evidence of liver and kidney damage, but no electrolyte abnormalities. With aggressive treatment, including furosemide and sodium bicarbonate, his kidney and liver function returned to normal, he survived the ordeal and was discharged. The group leaders took the third patient to a local ED, where cellulitis was diagnosed and oral antibiotics were prescribed. The pain and fever increased, and significant discoloration began spreading up her hand over the next 24 hours. The second ED visit resulted in an admission. When the findings progressed despite i.v. antibiotics, surgical exploration was performed with drainage, debridement of devitalized tissue and a change in i.v. antibiotics. The common feature of all of these conditions is pain out of proportion to few, if any, findings on physical examination. Swelling that causes much of the damage in each condition is frequently not appreciated clinically until the condition is well advanced. Remember, what you see is not necessarily what you get.

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Prolonged immobilization or physical inactivity has been shown to produce increased bone resorption due to enhanced osteoclastic activity and diminished bone formation. These skeletal changes are a typical complication in tetraplegic patients, who are at risk of developing hypocalcemia. Hypercalciuria is the most characteristic symptom. However, some patients develop hypercalcemia, which is infrequent in these patients, and the hypercalcemia can become a life-threatening complication. Until now, it has been unclear why a small percentage of immobilized patients develop hypercalcemia. Here we present a case of symptomatic hypercalcemia (serum calcium: 3.5 mM/l) following immobilization due to a critical illness polyneuropathy. The diagnosis could be established after malignant hypercalcemia, primary hyperparathyroidism, and other causes of hypercalcemia were excluded. Treatment with intravenous saline, furosemide, and calcitonin was not effective in lowering serum calcium. Treatment with pamidronate (Aredia) was successful and reduced the serum calcium to normal values.

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Patients receiving long-term treatment with torasemide had a lower hospitalisation rate (3.6%) compared to patients on furosemide (5.4%). Corresponding hospitalization rates in the German study were 1.4% under torasemide and 2% under furosemide. The higher hospitalisation rates in Swiss patients could be explained by a higher average age (75 years vs. 69 years) and a longer duration of symptomatic heart failure (4.1 yrs vs. 0.7 yrs). Cost estimates based on the average number of hospital days (0.54 under torasemide compared to 1.05 under furosemide) indicated that the financial burden could be halved by a long-term torasemide treatment.

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Therapeutic benefit that can be induced by a pharmaceutical compound partly relies upon the profile of its biological action. Evaluation of the drug-induced effect profile in a given pathological condition begins with the determination of the relevant biological effect related to the therapeutic benefit, which is not always obvious. Evaluation itself is based on dose-effect relationships as a function of time. During chronic treatment, such a kinetic profile oscillates between peak and trough levels. Relationships that can be established between time-dependent effect profile and pharmacokinetic data lead to PK-PD mathematical model, whose main objectives are simulation, prediction of effect and ultimately dose optimisation. The therapeutic implications of the time-dependent effect profile are well illustrated in the cases of antibiotics, diuretics such as furosemide and anti-hypertensive drugs. During drug development, PK-PD approaches can be used in the initial clinical and even pre-clinical phases and can lead to a better definition of effective dose ranges, optimisation of large scale clinical trials or identification of high risk patients. This may favour a reduction of costs and duration of development. Validation of such an approach is easier in well known therapeutic domains but can be more difficult with innovative drugs. The implications of PK-PD approaches can however, be, limited when the relevant biological or clinical parameter cannot be assessed, when the cascade of events leading to pharmacological and therapeutic effects is complex or finally when such PK-PD models require a long time to be established during the early phase of drug development.

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3 mg lasix 2016-01-24

We have used continuous infusion of furosemide to achieve diuresis in patients who are stable but hemodynamically compromised after heart operations. With a loading dose of 20 mg and a continuous infusion of 4 to 10 mg of furosemide per hour, mean 24-hour urine output was 5.7 L (238 +/- 65 mL/h). Potassium replacement was 115 +/- 20 mmol [115 +/- 20 mEq/L]. Cardiac index buy lasix online , central venous pressure, and diastolic pulmonary artery pressure did not change significantly, even though hemodynamic support was decreased in each patient. Continuous furosemide infusion is a simple, effective, and reliable method to achieve diuresis in select patients.

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We detected a known gain-of-function mutation in CASR in both the patient and her mother. Diuretic tests revealed a response to furosemide and no reaction to thiazide in the buy lasix online patient, although the mother responded well to both diuretics. CaSR co-localized with the Na(+)-Cl(-) cotransporter (NCCT) on distal tubular epithelial cells.

lasix gtt dosage 2015-09-16

To evaluate the metabolic effects of two anti-hypertensive agents with different actions, nifedipine 20 mg twice daily and furosemide 60 mg twice daily, 23 patients with untreated essential hypertension performed a double-blind, cross-over study in treatment periods of 5 months. Metabolic effects were evaluated by serum lipoprotein determinations, the intravenous glucose tolerance test and the hyperinsulinaemic euglycaemic clamp technique. Nifedipine and furosemide reduced blood pressure to the same extent (-14 to -15 mm Hg for supine SBP and -9 to -10 mm Hg for supine DBP, both P < 0.0001). Whereas both drugs significantly increased the levels of glycolysated haemoglobin (HbA1c, +0.24%, P < 0.005 for nifedipine buy lasix online and +0.43%, P < 0.001 for furosemide), only furosemide increased fasting blood glucose (+0.3 mmol/L, P < 0.01) and fasting insulin (+2.2 mU/L, P < 0.05) but impaired the early insulin response to i.v. glucose (-15 mU/L, P < 0.05). Insulin sensitivity on the other hand was significantly impaired by nifedipine treatment only (-1.6 mg/kg/min, P < 0.01). Whereas treatment with nifedipine did not change serum lipids, furosemide caused an increase in serum cholesterol (+0.2 mmol/L, P < 0.05) because of a rise in the LDL fraction (+0.32 mmol/L, P < 0.001). The insignificant change in heart rate induced by nifedipine treatment correlated with the change in HbA1c (r = 0.50, P = 0.05) and was inversely related to the change in insulin sensitivity (r = -0.56, P < 0.05). In conclusion, both furosemide and nifedipine caused abnormalities in glucose metabolism. In the nifedipine group the effects on glucose metabolism were related to the occurrence of tachycardia suggesting that sympathetic nerve activation could be involved in the metabolic impairments.

lasix brand name 2017-02-02

To identify all interventions that increase or buy lasix online reduce mortality in patients with acute kidney injury (AKI) and to establish the agreement between stated beliefs and actual practice in this setting.

lasix normal dose 2016-05-19

When a photochemically-induced infarct was produced in the right cortex of rats, tissue water content was increased markedly 4 and 24 h later (control: 79.00 +/- 0.08% ischaemia, 24 h: 82.96 +/- 0.15%). The left cortex was unaffected. Chlormethiazole (200 mg/kg i.p.) injection 5 min after onset of ischaemia decreased the oedema (ischaemia/chlormethiazole, 24 buy lasix online h: 82.16 +/- 0.21%, P < 0.01). At 24 h, ischaemic tissue Na+ content was increased (61%) and the K+ content decreased (9%). The Na+/K+ ratio therefore increased significantly (P < 0.001), a change that was diminished by chlormethiazole administration (P < 0.02). Chlormethiazole (1 mM), unlike furosemide (5 mM), did not reduce swelling of C6 glioma cells in hypotonic medium. The data suggest that chlormethiazole decreases oedema in this stroke model because of its neuroprotective properties and not because of an effect on anion transport.

lasix cost 2015-04-07

This study was designed to determine the protective effects of alpha-hederin on chemical-induced liver injury in CF-1 mice and to evaluate cytochrome P450 suppression by alpha-hederin as a means of protection. alpha-Hederin pretreatment (30 mumol/kg, sc x 3 days) protected mice from acetaminophen-, bromobenzene-, carbon tetrachloride-, furosemide-, and thioacetamide-induced liver injury, without affecting the hepatotoxicity of chloroform and dimethylnitrosamine. To examine the role of P450 in hepatoprotection by alpha-hederin, liver microsomes were prepared 24 hr following the last dose of alpha-hederin treatment (10 and 30 mumol/kg, sc x 3 days). Treatment of mice with alpha-hederin produced a dose-dependent suppression of liver cytochrome P450 (30-50%) and cytochrome b5 (20-30%) levels, as well as NADPH-cytochrome c reductase activity (15-25%). alpha-Hederin buy lasix online treatment also decreased the activities of P450 enzymes, such as 7-ethoxyresorufin O-dealkylation (65%), 7-pentoxyresorufin O-dealkylation (50%), coumarin 7-hydroxylation (40%), 7-ethoxycoumarin O-deethylation (45%), caffeine N3-demethylation (30-50%), chlorzoxazone 6-hydroxylation (35-55%), and the oxidation of testosterone to 2 alpha-, 6 alpha-, 15 alpha-, 15 beta-, 16 alpha-, 16 beta-, and 18/12 alpha-hydroxyltestosterone, androstenedione, and 6-dehydroxytestosterone (25-60%). Consistent with these observations, the levels of CYP1A, CYP2A, and CYP3A enzymes were also suppressed, as determined by immunoblotting with antibodies against rat P450 enzymes. These results demonstrate that treatment of mice with alpha-hederin decreases the levels and activities of several P450 enzymes. The suppression of P450 appears to be one of mechanisms by which alpha-hederin protects mice from the hepatotoxicity of some chemicals.

lasix 30 mg 2017-05-23

Due to their location on the luminal side of tubular cells, NCC and NKCC2 are well represented in UE proteome. The NCC signal is significantly decreased/absent in UE of Gitelman patients compared with control subjects (Mann-Whitney t-test, P < 0.001) and, similarly, the buy lasix online NKCC2 in those of Bartter type 1 (P < 0.001). The difference in the levels of the two proteins allows recognition of Gitelman and Bartter type 1 patients from controls and, combined with clinical data, from other Bartter patients. Moreover, the receiver operating characteristic curve analysis using UE NCC densitometric values showed a good discriminating power of the test comparing GS patients versus controls and BS patients (area under the curve value = 0.92; sensitivity 84.2% and specificity 88.6%).

lasix fluid pill 2017-12-06

We report the case of a patient buy lasix online treated with valpromide who presented edema of the lower limbs. The increase in furosemide dose allowed regression of edema, and valpromide discontinuation resulted in rapid normalization. Recurrence of mood disorders led to the reintroduction of valpromide, which was associated with recurrence of edema. The definitive withdrawal of valpromide resulted in resolution of edema.

lasix tablets 2017-05-16

The present in vitro microperfusion study examined whether furosemide has an effect on hydraulic conductivity (Lp X 10(-6) cm/sec.atm) and 14C-urea permeability (Pu X 10(-5) cm/sec) in inner medullary collecting ducts (IMCD) and cortical collecting tubules (CCT) isolated from rat and rabbit kidneys. Furosemide added to the bath fluid decreased arginine-vasopressin (AVP)-stimulated Lp of rat IMCD in a dose-dependent manner, with the threshold effect at 10(-6) M. Furosemide (10(-4) M) reduced Lp from 20.5 +/- 2.3 to 12.1 +/- 1.2 (P less than 0.01) reversibility, but had no effect when added to the perfusate. In addition, furosemide reduced dibutyryl cyclic AMP-stimulated Lp from 20.3 +/- 1.1 to 11.2 +/- 1.6 (P less than 0.01). This effect of furosemide was also observed with indomethacin, a PGE2 synthesis inhibitor. The addition of indomethacin (10(-4) M) to AVP (50 microU/ml) increased Lp from 24.7 +/- 2.3 to 29.7 +/- 2.8 (P less than 0.001), which was reduced to 20.3 +/- 2.6 (P less than 0.001) when furosemide was added to indomethacin in the bath. The inhibitory effect of furosemide on AVP-stimulated Lp was also observed in rabbit IMCD (Lp decreased from 12.8 +/- 0.8 to 5.15 +/- 1.46, P less than 0.02), but it was not observed in the CCT isolated from rabbit kidneys (7.96 +/- 1.87 with AVP vs. 7.94 +/- 1.41 with AVP + furosemide). Furthermore, in rat IMCD the stimulatory effect of AVP on Pu from 7.7 +/- 0.4 to 26.8 +/- 1.3 was reduced by furosemide to 19.7 +/- 1.2 (P less than 0.01).(ABSTRACT buy lasix online TRUNCATED AT 250 WORDS)

lasix 80 mg 2015-11-27

Chloride transport in 24-h primary cultures of human and rabbit distal colonic crypt cells (90 +/- 5% viable) were characterized using the Cl(-)-sensitive fluorescent probe 6-methoxyquinolyl acetoethyl ester. To calculate the Cl- influx in millimolar per second, the Stern-Volmer quenching constant was determined to buy lasix online be 24.3 M-1 for human and 24.6 M-1 for rabbit colonocytes. Cl- influx was dependent on extracellular Cl- concentration ([Cl-]0), with maximal influx at [Cl-]0 > or = 20 mM. The adenosine 3',5'-cyclic monophosphate (cAMP)-dependent secretagogues forskolin (1 microM), prostaglandin E1 (1 microM), and 8-bromoadenosine 3',5'-cyclic monophosphate (100 microM) increased Cl- influx in human colonocytes from 0.35 +/- 0.08 to 2.14 +/- 0.65, 1.85 +/- 0.51, and 0.84 +/- 0.04 mM/s (n = 4), respectively, and in rabbit colonocytes from 0.22 +/- 0.03 to 1.04 +/- 0.11, 1.24 +/- 0.12, and 1.08 +/- 0.07 mM/s (n = 5), respectively. Depending on the secretagogue, this influx was inhibited 50-90% by the Cl- channel blocker diphenylamine-2-carboxylate (DPC; 50 microM) and > or = 65% by the Na-K-2Cl cotransport inhibitor furosemide (10 microM). Phorbol 12,13-dibutyrate, an activator of protein kinase C, increased Cl- permeability 3.8-fold in human and 2.4-fold in rabbit colonocytes. The phorbol 12,13-dibutyrate-stimulated Cl- permeabilities were sensitive to DPC and furosemide but not to indomethacin. These studies demonstrate DPC and furosemide-sensitive Cl- permeabilities in isolated cultured human and rabbit colonocytes, which can be activated by cAMP and protein kinase C stimulators.

lasix and alcohol 2017-09-29

Criteria for cochlear implantation keep expanding and people with substantial residual low-frequency hearing are considered candidates for implantation nowadays. Therefore, electro-acoustical stimulation in the same ear (EAS) is receiving increasing interest. We have investigated the effects of intracochlear electrical stimulation on acoustically evoked auditory-nerve activity, using a forward masking paradigm. The stimulation electrode was placed in the basal turn of the cochlea. Compound action potential (CAP) recordings were performed in guinea pigs with severe high-frequency hearing loss and in normal-hearing control animals. In normal-hearing animals, electrical stimulation generally suppressed CAPs, especially at high acoustic frequencies (8 and 16 kHz) and low sound levels. At low frequencies (0.5 and 1 kHz), suppression was observed only at high sound levels. In animals with a high-frequency hearing loss, suppression of CAPs at low frequencies was substantially less compared to control animals, buy lasix online even at high current levels and temporal overlap of acoustic and electric stimuli. Hence, effects of electrical stimulation substantially differed between normal-hearing animals and animals with a high-frequency hearing loss. These findings stress the need for a proper animal model when investigating EAS. We conclude that in case of high-frequency loss, the basal part of the cochlea can be stimulated electrically with little effect on responses to low-frequency acoustic stimuli.

lasix 500 mg 2016-11-21

There is buy lasix online a significant heterogeneity in selecting an intervention based on PAC data among intensivists. The presence of Echo information may change the intervention selected but does not reduce heterogeneity. Any randomized trial evaluating efficacy of PAC's will have to have strict treatment protocols.

lasix buy online 2017-05-31

An aqueous extract of Sclederma of Poria cocos (hoelen) (2.4 g/kg/d, 1.2 g/kg/d or 0.6 g/kg/d) or furosemide (20 mg/kg/d) was administered orally to male Sprague-Dawley rats starting on the day of coronary ligation. The urine output of all rats was quantified and collected every day for 1 or 4 weeks. buy lasix online The expression of aquaporin-2 (AQP2) was examined after treatment for 1 or 4 weeks.

lasix 600 mg 2017-04-24

An adequate diuretic response is present in the neonatal period using MAG3 and this allows for reliable diagnosis of obstruction. An unobstructed or indeterminate result necessitates follow-up imaging to ensure obstruction does not develop. Co-existing VUJ buy lasix online obstruction may be missed in a scan showing PUJ obstruction.

lasix max dose 2017-08-12

The risk of hospitalization during 6 months in the patients receiving angiotensin-converting enzyme inhibitors at a dose of 25% or less of the therapeutic one was 21.18% (odds ratio (OR), 1.41; 95% confidence interval (CI), 1.13-1.76), that at doses of 50 and 100% of the therapeutic one was 16% (OR, 0.71; 95% CI, 0.56-0.88) and 34% ( Cialis 30 Mg OR, 0.51; 95% CI, 0.43-0.60), respectively. The risk of rehospitalization in the patients taking β-blockers at doses of 25, 50, and 100% of the therapeutic one was 26% (OR, 1.05; 95% CI, 0.94-1.17), 23% (OR, 0.902; 95% CI, 0.75-1.07), and 6.25% (OR, 0.19; 95% CI, 0.07-0.56), respectively. The combined analysis of the dose and use frequency of diuretics showed that the highest risk of rehospitalization turned was noted in the patients using a single dose of 100 mg of furosemide (4.2% of cases) once weekly and was as high as 39% (OR, 0.45; 95% CI, 1.04-1.98).

lasix gtt dose 2016-09-10

Stressors evoke a well-studied physiological stress-response, namely, an immediate systemic release of catecholamines from the adrenals followed shortly afterwards by the release of adrenal steroids. The intensity of that response can often be inferred by the amount of adrenal steroids released into the circulatory system. It is still unclear however how the intensity and duration of the stressor affect a number of brain regions, including those in the motivational system. The present study sought to determine whether a brief stressor, such as an isotonic saline injection, activated the brain's motivational system in mesolimbic regions compared with Cordarone Cost a more intense stressor exemplified by pharmacological challenges caused by the administration of a diuretic. Adult male Sprague-Dawley rats were either injected (s.c.) with isotonic saline or 5mg of the diuretic, furosemide. Controls did not receive any injections. Animals were sacrificed at 30, 60, 120, and 240 min after injection and trunk blood and brains were collected. Serum corticosterone and aldosterone levels were assessed through radioimmunoassay and mesolimbic brain activity was determined through in situ hybridization of mRNA expression of the immediate-early gene egr-1 in the caudate-putamen and nucleus accumbens. While both adrenal steroids demonstrated an initial peak in both stress groups, levels were higher and longer lasting in rats treated with furosemide. Interestingly, egr-1 mRNA levels were significantly higher only in the furosemide-treated group compared with controls. These findings suggest that a selective activation of motivational circuits occurs under thirst and salt-appetite-induced conditions such as those caused by diuresis.

lasix oral medication 2015-04-21

The influence of enteric nerves on intestinal ion and sugar transport was investigated in 3- to 4-wk-old suckling mice. Whole thickness segments of jejunum were mounted as flat sheets in flux chambers equipped to electrically stimulate nerves in the intestinal wall. Tetrodotoxin significantly reduced basal short-circuit current in a subset of tissues containing 3-O-methylglucose in the mucosal bath. Electrical field stimulation of intrinsic nerves evoked an increase in short-circuit current of 86 +/- 15 microA/cm2 that was due to an increase in active chloride secretion with no significant change in the net movement of other ions. The secretory response to neural stimulation was abolished by tetrodotoxin and reduced by the muscarinic antagonist, atropine. Mucosal-to-serosal fluxes of 3-O-methylglucose were not altered by the cholinergic agonist carbachol. Zanaflex 20 Mg These results show that ion transport in the suckling mouse jejunum is regulated by the enteric nervous system. Neural stimulation evokes a chloride secretory response that is mediated by acetylcholine and other noncholinergic transmitters. Sugar transport in the murine small intestine does not appear to be influenced by muscarinic cholinergic agonists.

lasix 60 mg 2016-01-27

All Thoroughbreds (n = 22,589) that finished a race on dirt surfaces at tracks in the United States and Canada between June 28 and July 13, 1997 in jurisdictions that allowed the Lioresal Tabs use of furosemide.

lasix 3169 pill 2015-08-22

Prospective Risperdal Iv Dose non-blinded pharmacokinetic-pharmacodynamic study.

lasix generic brand 2017-02-24

Propranolol, a Vantin Tab beta-adrenergic blocker, is used in the treatment of a large number of cardiovascular diseases such as hypertension and arrhythmias. Propranolol, in combination with furosemide, is used to treat hypertensive disorders although their side effect profile is not very obvious. In present study, the effects of the drugs furosemide and propranolol were in corporately investigated both on glutathione homeostasis and their antioxidant effect on ACHN cells.

lasix drug interactions 2016-07-18

The synthesis of adenosine triphosphate (ATP) depends on the coordinated interaction of oxygen delivery and glucose breakdown in the Krebs cycle. Cellular oxygen depots are non-existent, therefore the peripheral cells are totally dependent on the circulation for sufficient oxygen delivery. Shock is the clinical manifestation of cellular oxygen craving. The commonly measured variables--blood pressure, heart rate, urinary output, cardiac output and systemic vascular resistance--are not sensitive or accurate enough to warn of impending death in acutely ill patients nor are they appropriate for monitoring therapy. Calculated oxygen transport and oxygen consumption parameters provide the best available measures of functional adequacy Bystolic Cost Usa of both circulation and metabolism. In order to optimise oxygen delivery (DO2), 4 interacting factors must be taken into account: cardiac output, blood haemoglobin content, haemoglobin oxygen saturation and avidity of oxygen binding to haemoglobin. For viscosity reasons, the optimal haemoglobin concentration is in the vicinity of 90 to 100 g/L, but for optimising the oxygen transport 100 to 115 g/L or a haematocrit of 30 to 35% seems better. The p50 (the pO2 at which haemoglobin is 50% saturated) describes the oxygen-haemoglobin dissociation curve; normally its value is +/- 27 mm Hg. It can be influenced by attaining normal body temperature, pH, pCO2 and serum phosphorous levels. In order to obtain an arterial blood saturation (SaO2) of more than 90% with acceptable haemodynamics, the ventilation mode and inspired oxygen fraction (FiO2) must be adapted; care must be taken not to stress the labile circulation with haemodynamic compromising ventilation techniques [e.g. high positive end expiratory pressure (PEEP) levels, inverse-ratio ventilation, etc.]. The factor most amenable to manipulation is the cardiac output, with its 4 determinants--preload, afterload, contractility and heart rate. In daily clinical practice, heart rate should be between 80 and 120 beats/min; small variations are acceptable. Important deviations must be treated by chemically [isoprenaline (isoproterenol)] or electrically (pacing techniques) accelerating the heart, or with the different antiarrhythmic drugs. A wide variety of agents is available to decrease the preload: diuretics [especially furosemide (frusemide)], venodilators like nitroglycerin (glyceryl trinitrate), isosorbide dinitrate (sorbide nitrate) and sodium nitroprusside, ACE inhibitors, phlebotomy, and haemofiltration techniques (peritoneal or haemodialysis, continuous arteriovenous haemofiltration). To increase the preload, volume loading using a rigid protocol ('rule of 7 and 3'), preferably with colloids, or vasopressor agents [norepinephrine (noradrenaline), epinephrine (adrenaline), dopamine] are useful. Arterial vasopressors are needed to improve perfusion pressure of 'critical' (coronary and cerebral) arteries. Afterload can be decreased by arterial vasodilators. Predominantly arterial dilators are hydralazine and clonidine, while sodium nitroprusside, nitroglycerin and isosorbide dinitrate have combined arterial and venous dilating actions.(ABSTRACT TRUNCATED AT 400 WORDS)

lasix 5 mg 2015-12-09

Eight pigs underwent total hepatectomy after Y-graft interposition between the infrahepatic vena cava and the portal vein to the suprahepatic vena cava. An intracranial probe was inserted for intracranial pressure (ICP) monitoring. Animals received pressure-controlled ventilation under deep narcosis. Vital parameters were continuously recorded. Urinary output, blood gas analysis, haemoglobin, hematocrit, serum electrolytes, lactate, and glucose were monitored hourly, and creatinine, prothrombin time, international normalised ratio, and serum albumin were monitored every 8 hours. Sodium chloride solution 0.9 Prandin Dosing %, hydroxyethyl starch 6%, fresh frozen plasma, and erythrocyte units were used for volume substitution, and norepinephrine was used to prevent severe hypotension. Serum electrolytes and acid-base balance were corrected as required. Antibiotic prophylaxis with ceftriaxon was given daily, as well as furosemide, to maintain diuresis.

lasix online 2015-12-17

In brain slices from young (postnatal day (P) 10--15) rat somatosensory cortex, real-time neuronal intracellular Cl(-) concentration ([Cl(-)](i)) recordings were made by an optical technique measuring 6-methoxy-N-ethlquinolinium iodide (MEQ) fluorescence. Oxygen--glucose deprivation (in vitro model of ischemia) induced a long-lasting [Cl(-)](i) increase preceded by a rapid, transient [Cl(-)](i) decrease that could not be inhibited by blockers of Cl(-) pumps, Cl(-) channels, or Cl(-) antiporters, but was sensitive to cation-Cl(-) cotransporter inhibitors (bumetanide and furosemide). Use of low external Na(+) or high external K(+) revealed that the Na(+),K(+)-2Cl(-) cotransporter was inhibited by bumetanide and furosemide, whereas the K(+)-Cl(-) cotransporter was preferentially inhibited by furosemide under our experimental conditions. With a reduced inward driving force for Na(+) (reducing Na(+),K(+)-2Cl(-) cotransport), the transient [Cl(-)](i) decrease was only rarely induced by oxygen-glucose deprivation. In contrast, with a reduced outward driving force for K(+) (reducing K(+)-Cl(-) cotransport), the transient [Cl(-)](i) decrease still occurred. These results suggest that the transient [Cl(-)](i) decrease was primarily mediated by a rapid inhibition of the inwardly directed Na(+),K(+)-2Cl(-) cotransporter. Reverse transcriptase-polymerase chain reaction (RT-PCR) experiments suggested that the isoform involved is NKCC1. We hypothesize that the initial rapid Cl(-) efflux might effectively delay the irreversible Cl(-) influx that mediates neuronal injury.

lasix 80mg tab 2015-11-13

Since in whole animal studies and in man the renal clearance of cimetidine was prolonged by the coadministration of probenecid, the aim of the present study was to examine the interaction of the organic base cimetidine with the organic anion transport system at the basolateral membrane of isolated non-perfused rabbit proximal tubules. S2 segments of proximal tubules were incubated at 37.5 degrees C with 3H-cimetidine (2 x 10(-7) mol/l) or 3H-PAH (4 x 10(-6) mol/l, as a marker for the organic anion transport system) and 14C-inulin (marker for the extracellular space) for 25 min to achieve a steady state. Afterwards, a nonradiolabelled substance was added to the bath, and the change of the cellularly stored radioactivity was measured at 5-min intervals. Probenecid (5 x 10(-5) mol/l) decreased the cellular amount of 3H-cimetidine to 26% of the control value. At this concentration, furosemide and Na2SO4 had no effect. At a concentration of 10(-3) mol/l, these substances reduced the cellular 3H-cimetidine uptake to 33% (furosemide) and 57% (Na2SO4) of the control value. 10(-4) and 10(-3) mol/l succinate diminished the steady-state uptake of cimetidine to 77% and 53% of the control value, respectively. On the other hand, cimetidine (10(-3) mol/l) decreased the cellular uptake of 3H-PAH to 52% of the control value. N1-methylnicotinamide (5 x 10(-5) mol/l and 10(-3)mol/l) had no effect on the steady-state uptake of 3H-PAH. These results indicate that the organic base cimetidine, besides its high affinity for the cation transporter, also interacts with the organic anion transport system at the basolateral membrane of rabbit proximal tubules.

lasix 100 mg 2016-12-27

The authors reviewed the findings of Doppler ultrasonography and diuretic renal scintigraphy performed over a 3-year period for 27 pyelocaliectatic kidneys (17 obstructed and 10 unobstructed) in 20 individuals ranging in age from 19 to 88 years. The kidneys were classified as "obstructed" or "unobstructed" on the basis of the resistive index as calculated from Doppler ultrasonographic results and as "obstructed", "unobstructed" or "indeterminate" on the basis of the clearance half-time determined from scintigraphic findings.

lasix 300 mg 2016-03-26

In ICU patients, 60 mg FU mixed with HA or FFP has a similar diuretic effect in patients with CCr >20 ml/min. FFP is an effective alternative choice for improving diuresis for ICU patients with hypoalbuminemia. In patients with CCr < or = 20 ml/min, albumin mixed with 60 mg FU has a superior diuretic effect compared with FFP mixed with FU.

300 mg lasix 2017-05-28

To review the clinical pharmacology of torsemide and to compare it with currently available loop diuretics, particularly furosemide.