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PubMed1995

Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy.

PURPOSE: We have previously found thiamine (vitamin B1) deficiency in patients with congestive heart failure (CHF) who had received long-term furosemide therapy. In the present study, we assessed the effect of thiamine repletion on thiamine status, functional capacity, and left ventricular ejection fraction (LVEF) in patients with moderate to severe CHF who had received furosemide in doses of 80 mg/d or more for at least 3 months. PATIENTS AND METHODS: Thirty patients were randomized to 1 week of double-blind inpatient therapy with either i.v. thiamine 200 mg/d or placebo (n = 15 each). All previous drugs were continued. Following discharge, all 30 patients received oral thiamine 200 mg/d as outpatients for 6 weeks. Thiamine status was determined by the erythrocyte thiamine-pyrophosphate effect (TPPE). LVEF was determined by echocardiography. RESULTS: TPPE, diuresis, and LVEF were unchanged with i.v. placebo. After i.v. thiamine, TPPE decreased (11.7% +/- 6.5% to 5.4% +/- 3.2%; P < 0.01). LVEF increased (0.28 +/- 0.11 to 0.32 +/- 0.09; P < 0.05), as did diuresis (1,731 +/- 800 mL/d to 2,389 +/- 752 mL/d; P < 0.02), and sodium excretion (84 +/- 52 mEq/d to 116 +/- 83 mEq/d, P < 0.05). In the 27 patients completing the full 7-week intervention, LVEF rose by 22% (0.27 +/- 0.10 to 0.33 +/- 0.11, P < 0.01). CONCLUSIONS: Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy.

Aged↗

PubMed2002

Effects of barium, furosemide, ouabaine and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) on ionophoretically-induced changes in extracellular potassium concentration in hippocampal slices from rats and from patients with epilepsy.

Glial cells limit local K(+)-accumulation by K(+)-uptake through different mechanisms, sensitive to Ba(2+), ouabaine, furosemide, or DIDS. Since the relative contribution of these mechanisms has not yet been determined, we studied the effects of bath-applied barium (2 mM), ouabaine (9 microM), furosemide (2 mM), and DIDS (1 mM) on ionophoretically-induced rises in [K(+)](o) in the pyramidal layer of area CA1 from normal rat slices, in the presence of glutamate receptor (Glu-R) antagonists. We also investigated the effect of barium on ionophoretically-induced tetrapropylammonium (TPA(+))-signals in order to test for barium-induced changes of the extracellular space. Finally, we repeated the barium experiment on slices from human non-sclerotic and sclerotic hippocampal specimens to assess a reduced glial capability for barium-sensitive K(+)-uptake in sclerotic tissue from epilepsy patients. In normal rat slices barium augmented ionophoretically-induced rises in [K(+)](o) by approximately 120%, also in the presence of tetrodotoxin (TTX) (by approximately 150%), but did not significantly affect the TPA(+)-signal. Ouabaine also augmented the K(+)-signal, but only by 27%. Furosemide and DIDS had negligible effects. In slices from sclerotic human hippocampus an augmentation of the K(+)-signal by barium was absent. Thus barium augments ionophoretically-induced K(+)-signals to a similar extent as previously shown for stimulus-induced signals. We suggest that glial barium-sensitive K(+)-buffer mechanisms reduce fast local rises of [K(+)](o) by at least 50%. This capability of glial cells is extremely reduced in area CA1 of slices from human sclerotic hippocampal specimens.

2-Amino-5-phosphonovalerate↗

PubMed1997

Furosemide does not prevent indomethacin-induced renal side effects in preterm infants.

OBJECTIVE: To determine whether furosemide could prevent renal side effects of indomethacin (INN, indometacin) used for the pharmacologic closure of the patent ductus arteriosus (PDA) in preterm infants. METHODS: Thirty-six preterm infants with birth weights < 1750 gm affected by hemodynamically significant PDA were randomly assigned to one of two study groups. Group 1 consisted of 18 infants treated with three doses of indomethacin (0.20 mg/kg every 12 hours); each dose was followed by a dose of furosemide (1 mg/kg). Group 2 consisted of 18 infants treated only with the same doses of indomethacin. Body weight, urine output, glomerular filtration rate (GFR), fractional excretion of sodium (FENa+) and potassium (FEK+), and osmolal and free water clearance were evaluated in both groups before, during, and after treatment. RESULTS: The body weight trend, serum sodium, chloride and potassium concentrations, plasmatic and urinary osmolality were similar during the treatment in both the groups. A significant reduction of urine output (p < 0.01) was detected in group 2 but not in group 1. A significant increase of blood urea nitrogen and serum creatinine was detected at the end of treatment in group 1 compared with group 2. During the treatment, a significantly higher GFR (p < 0.05) was found in group 2 than in group 1. FENa+ and FEK+ were significantly higher (p < 0.05 and p < 0.001, respectively) in group 1 than in group 2 during and after the treatment. The osmolol clearance and free water clearance were significantly higher during and after treatment (p < 0.01 and p < 0.001, respectively) in group 1 than in group 2. CONCLUSIONS: Our findings show that furosemide cannot prevent the indomethacin-induced renal failure, but it does not have any negative influence on its therapeutic effectiveness.

Body Weight↗

PubMed2003

Photostability studies on the furosemide-triamterene drug association.

The photostability of the diuretic drugs triamterene and furosemide, individually and combined, was evaluated. Spectrophotometric, spectrofluorimetric and chromatographic (HPLC) methods were applied to monitor the drug photodegradation. Furosemide was confirmed to be highly photolable in both pH 7.4 solution and methanol. Differently triamterene proved to be highly fluorescent (emission quantum yield: 0.9 in methanol and 0.8 in pH 7.4 solution), but essentially photostable (photochemical reaction quantum yield: congruent with 5 x 10(-4)) under exposure at 365 and 313 nm radiations. When the combined drugs in pH 7.4 solutions were exposed to 365 nm radiations a significant photoprotective effect of triamterene on furosemide was observed. The photoreactivity of the drugs was exploited to develop an HPLC method involving a post-column on-line photochemical derivatization useful to confirm the analyte identity in a commercial dosage form (tablets). The commercial product, containing the combined drugs, proved to be photostable also after long (65 h) light exposure.

Chromatography, High Pressure Liquid↗

PubMed1999

Urinary thiamine excretion in the rat: effects of furosemide, other diuretics, and volume load.

Long-term furosemide therapy is associated with increased urinary loss of thiamine. To examine the mechanism of furosemide-induced urinary thiamine loss, we measured urinary excretion of thiamine in rats in response to increasing doses of furosemide, acetazolamide, chlorothiazide, amiloride, mannitol, and extracellular fluid (ECF) volume loading by saline infusion. All animals were in normal thiamine balance as reflected by a thiamine pyrophosphate effect (TPPE) of 2.25% +/- 0.60% (mean +/- SEM), and all had normal renal function. Urinary flow increased in response to diuretic administration in a dose-dependent manner, reaching (mean) peak urinary flow rates of 283 to 402 microL/min. Fractional excretion of sodium (FE(Na)) exhibited the same pattern, reaching peak values of 12.3% to 23.2%. Urinary thiamine excretion increased in proportion to the incremental doses of diuretic agents, reaching (mean) maximal values of 7.44 to 9.34 pmol/min, with no significant difference (P = .11) between the various diuretics tested nor in response to saline loading. None of the diuretics tested differed in the effect on thiamine excretion, which was clearly flow dependent and only partially related to fractional sodium excretion. Urinary flow rate, being the single significant predictor, explained 78% (R2 = 0.78) of the variability in thiamine excretion rates. These findings indicate that urinary thiamine loss is caused by a nonspecific, flow-dependent mechanism common to all of the diuretics tested.

Animals↗

PubMed1999

Urinary loss of thiamine is increased by low doses of furosemide in healthy volunteers.

Prolonged furosemide treatment is associated with urinary loss of thiamine and thiamine deficiency in some patients with congestive heart failure and low dietary thiamine intake. In the rat, diuretic-induced thiamine urinary loss is solely dependent on increased diuresis and is unrelated to the type of diuretic used. We studied the effects of single intravenous doses of furosemide (1, 3, and 10 mg) and of normal saline infusion (750 mL) on urinary thiamine excretion in 6 volunteers. Over a 6-hour period, furosemide induced dose-dependent increases in urine flow and sodium excretion rates (mean +/- SD), from 51 +/- 17 mL/h at baseline to 89 +/- 29 mL/h, 110 +/- 38 mL/h, and 183 +/- 58 mL/h (F = 10.4, P < .002) and from 5.1 +/- 2.3 mmol/h to 9.4 +/- 6.8 mmol/h, 12.1 +/- 2.6 mmol/h, and 20.9 +/- 10.6 mmol/h (F = 6.3, P < .005) for the three doses, respectively (104 +/- 35 mL/h and 13.0 +/- 6.2 mmol/h for the saline infusion). During this period the thiamine excretion rate doubled from baseline levels (mean of four 24-hour periods before the diuretic interventions) of 6.4 +/- 5.1 nmol/h to 11.6 +/- 8.2 nmol/h (F = 5.03, P < .01, for all four interventions, no difference being found between them), then returning over the following 18 hours to 6.1 +/- 3.9 nmol/h. The thiamine excretion rate was correlated with the urine flow rate (r = 0.54, P < .001), with no further effect of the type of intervention or sodium excretion rate. These findings complement our previous results in animals and indicate that sustained diuresis of >100 mL/h induces a nonspecific but significant increase in urinary loss of thiamine in human subjects. Thiamine supplements should be considered in patients undergoing sustained diuresis, when dietary deficiency may be present.

Adult↗

PubMed1976

Diuretic effect of furosemide in acute glomerulonephritis.

Twenty-five children with the diagnosis of acute glomerulonephritis were treated with oral or intravenous doses of furosemide. The intravenous administration of 1 mg/kg or greater resulted in an increase in urine volume in all patients. Oral doses of less than 2 mg/kg were not as effective, but there was wide variation in diuretic response to the drug. In 13 patients, plasma concentrations of furosemide were measured. The plasma half-life varied from 2.3 to 4.4 hours after intravenous administration of the drug. The plasma concentration of furosemide did not correlate with diuretic response.

Acute Disease↗

PubMed1998

Coadministration of theophylline enhances diuretic response to furosemide in infants during extracorporeal membrane oxygenation: a randomized controlled pilot study.

OBJECTIVE: This pilot study evaluates the efficacy of low-dose theophylline administered before furosemide to enhance diuresis in neonates recovering from fluid retention during extracorporeal membrane oxygenation (ECMO). STUDY DESIGN: Infants receiving ECMO (n = 24) were randomized (double blind, placebo-controlled) to receive either regimen A (placebo/furosemide day 1, theophylline/furosemide day 2, placebo/furosemide day 3) or regimen B (theophylline/furosemide day 1, placebo/furosemide day 2, theophylline/furosemide day 3). Urine flows and renal functions were compared. RESULTS: Urine flow rate before initiation of diuretic therapy was not significantly different between groups A and B (2.6 +/- 1.4 vs 3.5 +/- 1.3 ml/kg/hr, respectively, p = 0.12). Infants who received theophylline/furosemide had significantly higher urine flow rates than those who received placebo/furosemide on day 1 (11.8 +/- 4.6 vs 7.2 +/- 2.4 ml/kg/hr, p < 0.01). The 24-hour fluid volumes and balances became significantly more negative with theophylline enhancement of furosemide's effect. There were no significant differences in renal function between the two groups. CONCLUSION: Low doses of theophylline given before furosemide administration significantly enhance diuretic response in infants with fluid retention during ECMO.

Diuresis↗

PubMed1996

Renal Doppler ultrasound in children with obstructive uropathy: effect of intravenous normal saline fluid load and furosemide.

PURPOSE: We studied the effect of hyperhydration with normal saline and furosemide on renal resistive index in children with obstructive uropathy. MATERIALS AND METHODS: 99mTechnetium-mercaptoacetyltriglycine diuretic renography and Doppler ultrasound were done in 27 children (54 renal units) with unilateral or bilateral hydronephrosis. Doppler studies were performed at baseline, and after infusion of normal saline and administration of furosemide. Half-time drainage, considered the gold standard for the diagnosis of renal obstruction, was compared to resistive index. RESULTS: There was a positive correlation between half-time and resistive index on both Doppler studies. With a resistive index of 0.70 as the critical value for predicting renal obstruction 82 versus 100% sensitivity (p < 0.006), 63 versus 94% specificity (p < 0.04) and 76 versus 98% overall accuracy (p < 0.0005) were obtained for Doppler studies at baseline and after induced diuresis, respectively. All children with false-positive results were younger than age 4 years. CONCLUSIONS: Doppler ultrasonography after hyperhydration with normal saline and furosemide is an accurate method for diagnosing renal obstruction in children. It is more sensitive, specific and accurate than baseline Doppler studies.

Child↗

PubMed1984

Inhibition studies of microsomal UDP-glucuronosyltransferase activities by furosemide and salicylamide.

Contrarily to cytochrome P-450, a few inhibitors of UDP-glucuronosyltransferase have been described. We verified the nature of the in vitro inhibition due to furosemide, using 4 different aglycones (morphine, p-nitrophenol, borneol and eugenol) presumably belong may to different clusters of UDP-glucuronosyltransferase activities. The variations of these corresponding kinetic parameters (Km, Vmax, specific activities) must correspond to different inhibition mechanisms of furosemide, for example different site(s) of fixation in the area of the active site of UDPGT. Because these variations were not as classically described, we checked the impact of furosemide pretreatment on in vitro levels of different UDPGT activities. We compared these result, with another inhibitor (salicylamide). The apparent induction due to the both molecules enforced the hypothesis of a complexe inhibition mechanism.

Animals↗

PubMed1999

Pharmacoeconomic comparison of an albumin-furosemide complex versus sequential therapy for renal insufficiency.

The purpose of this economic analysis was to develop an economic model using intra-institutional cost data for acute, oliguric renal insufficiency treated with either an albumin-furosemide complex or albumin followed by furosemide (sequential therapy). The perspective of this study was from the standpoint of the institution (University Medical Center, a teaching hospital). The decision tree and sensitivity analyses demonstrated that the albumin-furosemide complex would be more effective and less costly than sequential therapy for a range of outcome probabilities. Using effectiveness assumptions from published literature, the complex could avoid dialysis in 27% of patients compared with 8% of patients receiving sequential therapy. The complex would also be less costly ($7778 vs $8748). In terms of cost-effectiveness, the complex is $28,807 per averted dialysis compared with $109,350 for sequential therapy.

Acute Disease↗

PubMed1994

Hemodynamic effects of acute administration of furosemide in patients with cirrhosis receiving beta-adrenergic antagonists.

In patients with cirrhosis, both beta-blockers and diuretics decrease the degree of portal hypertension. Since their mechanisms of action differ, the combination of these two substances should induce a more pronounced effect on portal pressure than one of these substances alone. Thus, the hemodynamic effects of furosemide were evaluated in ten patients with cirrhosis receiving beta-blockers. One hour after furosemide (0.75 mg/kg intravenously) administration, cardiac output decreased significantly from 6.2 +/- 0.6 to 5.2 +/- 0.3 l/min and blood volume from 8.0 +/- 1.6 to 5.3 +/- 0.5 l. Mean arterial pressure was not affected. Wedged and free hepatic venous pressures did not change significantly; nor did the hepatic venous pressure gradient (19.6 +/- 1.7 to 18.6 +/- 1.5 mmHg). Azygos blood flow was not affected (0.46 +/- 0.05 to 0.50 +/- 0.07 l/min). In conclusion, this study did not demonstrate that the addition of furosemide to propranolol further decreased portal pressure in patients with cirrhosis. The long-term effects of this combination are unknown and should be tested.

Adrenergic beta-Antagonists↗

PubMedDate not supplied

Na(+):K(+):ATPase mRNA expression in the kidney during adaptation to sodium intake and furosemide treatment.

Nephron tubular epithelium possesses the capacity of adaptation to any salt ingestion condition. The mechanism of adaptation is due in part to an increase in the activity of Na(+):K(+):ATPase at the basolateral membrane. The goal of the present study was to analyze the long-term regulation of the Na(+):K(+):ATPase alpha(1)-subunit mRNA expression during changes in NaCl metabolism. Male Wistar rats given a normal, high, or low NaCl diet, and intraperitoneal administration of the loop diuretic furosemide from 12 h to 7 days were studied. Rats were kept in metabolic cages 4 days before and throughout the study to determine daily urinary electrolyte excretion and osmolarity. At the end of each experimental period, creatinine clearance and serum electrolytes were also measured. Total RNA was extracted from each individual cortex or outer medulla and from pooled inner medullas using the guanidine/cesium chloride method. Na(+):K(+):ATPase alpha(1)-subunit mRNA expression was assessed by nonradioactive dot-blot analysis. Experimental maneuvers were well tolerated and all groups developed the appropriate renal response to each experimental condition. Urinary sodium excretion was significantly higher in rats administered a high sodium diet or furosemide and lower in rats treated with a low sodium diet after 7 days of treatment. Glomerular filtration rate was similar among all groups. However, the level of expression of the Na(+):K(+):ATPase alpha(1)-subunit did not change in any model. Nephron adaptation to the modification in NaCl intake or furosemide administration over 7 days did not include changes in Na(+):K(+):ATPase alpha(1)-subunit mRNA levels.

Adaptation, Physiological↗

PubMed1989

Protective role of furosemide and saline in radiocontrast-induced acute renal failure in the rat.

Acute renal failure (ARF) can be produced in rats by a combination of insults which augment transport activity and blunt regulatory mechanisms designed to maintain medullary oxygen sufficiency. This type of ARF is characterized by necrosis of medullary thick ascending limbs (mTALs). Uninephrectomized, salt-depleted rats injected with indomethacin (10 mg/kg) develop ARF following the administration of the radiocontrast agent, iothalamate. Furosemide (20 mg/kg, intravenous), administered immediately before the contrast material, attenuated the severity of ARF and reduced mTAL necrosis. Treatment with furosemide and/or normal saline prevented both the decline in renal function and mTAL injury. It is concluded that furosemide and normal saline may ameliorate the course of ARF if administered before radiocontrast.

Acute Kidney Injury↗

PubMed2001

A spectrophotometric-partial least squares (PLS-1) method for the simultaneous determination of furosemide and amiloride hydrochloride in pharmaceutical formulations.

A numerical method, based on the use of spectrophotometric data coupled to PLS-1 multivariate calibration, is reported for the simultaneous determination of furosemide and amiloride hydrochloride in synthetic samples and commercial tablets. The method was applied in the concentration ranges of 8.0-13.0 mg l(-1) for furosemide and 1.0-1.6 mg l(-1) for amiloride hydrochloride. Its accuracy and precision were determined, and it was validated by the analysis of synthetic mixtures of both drugs. The method was successfully applied to the quantitation of furosemide and amiloride hydrochloride in three different pharmaceutical formulations, providing results in agreement with those obtained by HPLC. It allowed the rapid, accurate and precise simultaneous estimation of the concentration of both analytes of interest in spite of their important spectral overlap, high concentration relationship and the presence of small amounts of different, unmodelled, absorbing excipients.

Amiloride↗

PubMed2003

Simultaneous high-performance liquid chromatographic assay of furosemide and propranolol HCL and its application in a pharmacokinetic study.

A practical, sensitive, selective and efficient reversed-phase high-performance liquid chromatographic (HPLC) method is reported for the determination of two commonly used antihypertensive drugs, furosemide and propranolol hydrochloride. The drugs were eluted through a Nucleosil C(18) column with a mobile phase composed of 0.02 M potassium dihydrogen phosphate and acetonitrile (80:20, v/v) adjusted to pH 4.5 and the effluent from the column was monitored at 235 nm. The present method enabled simple and isocratic HPLC with UV detection of these drugs in raw materials and in pharmaceutical formulations. These procedures were also applied for the assay of furosemide in rabbits' plasma, using propranolol hydrochloride as an internal standard. The linear concentration range of the assay was 0.1-200 and 5-200 microg ml(-1) for furosemide and propranolol hydrochloride, respectively. The inter and intra-day assay precision and accuracy showed reproducibility and good linearity (r(2)>0.99). The method retained its accuracy and precision when applying the standard addition technique. The results obtained by applying the proposed method was statistically analysed and compared with those obtained by the reported methods.

Animals↗

PubMed2002

Nebulized furosemide as a novel treatment for dyspnea in terminal cancer patients.

Three terminal cancer patients with severe dyspnea were treated with nebulized furosemide. The underlying causes of dyspnea varied. Twenty milligrams of furosemide was nebulized and inhaled four times each day. Dyspnea dramatically improved and could be controlled for weeks. No noticeable side effects were observed. Inhalation of nebulized furosemide seems to be an effective and useful treatment for dyspnea in terminal cancer patients, but these observations need to be confirmed in a randomized controlled trial.

Administration, Inhalation↗

PubMed2003

Effect of nebulized furosemide in terminally ill cancer patients with dyspnea.

We evaluated the effect of ultrasonically nebulized furosemide (20 mg) on dyspnea uncontrollable by standard therapy in patients with terminal cancer. Dyspnea was evaluated using the Cancer Dyspnea Scale (CDS) before and 60 min after inhalation. Changes in arterial blood gases, hemoglobin oxygen saturation (SpO2), heart rate (HR), and respiratory rate (RR) also were evaluated. In 12 of 15 patients (80%), total dyspnea scores by CDS improved significantly after inhalation of furosemide (P = 0.007), especially concerning a reduced sense of effort (P = 0.013) and reduced anxiety (P = 0.04). No significant changes were observed in the partial pressure of oxygen in arterial blood (PaO2), the partial pressure of carbon dioxide in arterial blood (PaCO2), SpO2, HR, or RR. Inhalation of nebulized furosemide appears to be effective against dyspnea in terminally ill cancer patients.

Chloride Channels↗