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PubMed2000

Gastrointestinal first-pass effect of furosemide in rats.

The first-pass effect of furosemide was investigated in rats. Furosemide intravenous solution (20 mg kg(-1) Lasix), was administered via the jugular vein and the portal vein, orally, and instilled directly into the duodenum of rats. The first-pass effects of furosemide by lung, heart, and liver seemed to be negligible in rats. The absolute bioavailability of furosemide was 28.9 and 48.3% after oral and intraduodenal administration, respectively. Based on the gastrointestinal (GI) recovery study, 68.3 and 69.5% of furosemide were found to have disappeared mainly due to absorption and/or metabolism from rat GI tract after oral and intraduodenal administration, respectively. The results indicate that gastrointestinal and intestinal first-pass effects of furosemide were approximately 40% (68.3-28.9%) and 20% (69.5-48.3%) of the dose, respectively.

Administration, Oral↗
PubMed1987

A study on furosemide disposition in man.

Furosemide disposition in man was studied. Six male young healthy volunteers were given 20 mg furosemide by bolus intravenous injection and 10, 20, 30 and 40 mg furosemide (solution) orally. The serum drug concentration was determined by high performance liquid chromatography and the urinary excretion was determined spectrophotometrically after diazotization. The experimental data from serum and urine samples were simultaneously subjected to computer analysis. On the basis of the results, it was demonstrated that disposition of furosemide in man can be described by a two-compartment open model with the following average parameters: t1/2 alpha = 0.237 +/- 0.069 h, t1/2 beta = 1.29 +/- 0.20 h and Vss = 8.46 +/- 2.171. After oral administration of furosemide solution, the drug was rapidly absorbed from the gastrointestinal tract with a first-order absorption rate constant ka of 2.33 +/- 0.93 h-1 but there was a lag time of about 6.45 min for drug resolution and entering the absorption site. The oral relative bioavailability was estimated as 83 +/- 14%, which was higher than reported values. The elimination of furosemide was very rapid and was mainly via the renal route. The systemic clearance (CLs) and renal clearance (CLr), following bolus intravenous dosing were 7.60 +/- 2.29 and 6.44 +/- 1.81 l/h, respectively. The oral route did not influence CLs and CLr on the whole, but the nonrenal clearance ratio (CRnr) after oral dosing (15.7 +/- 4.8%) was significantly higher than that after intravenous administration (11.2 +/- 4.0%), which can be explained by a first-pass effect of the liver-portal system.

Administration, Oral↗
PubMed1980

The effect of angiotensin II antagonist, Sar1-Ile8-angiotensin II, on furosemide-induced increase in plasma noradrenaline, renin activity and aldosterone in unanesthetized dogs.

In order to evaluate the role of the renin-angiotensin system and the sympathetic nervous system in the maintenance of blood pressure in the sodium-depleted state, the changes of plasma renin activity (PRA), plasma aldosterone concentration (PAC) and plasma noradrenaline (PNA) were examined in unanesthetized dogs after the administration of furosemide. Furthermore, the role of the renin-angiotensin system in the increased sympathetic nerve activity induced by furosemide was assessed by using Sar1-Ile8-angiotensin II, an angiotensin II antagonist. When a dose of 0.8 mg/kg of furosemide was injected intravenously, 3 times every 15 minutes, PRA and PNA were significantly increased with a concomitant increase in PAC. Sar1-Ile8-angiotensin II induced a significant increase in PAC and a slight increase in PRA, while no changes were found in PNA and the mean blood pressure. The increase in PNA induced by furosemide was inhibited dose-dependently by Sar1-Ile8-angiotensin II, through PRA and PAC were further increased. There results suggest that an administration of furosemide induced the increase in PNA and the increase in PNA by furosemide might by mediated by the renin-angiotensin system.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1990

The pharmacokinetics and pharmacodynamics of furosemide in anesthetized dogs with normal and experimentally decreased renal function.

The pharmacokinetics and the biliary and urinary excretions following intravenous administration of furosemide (5 mg/kg) were investigated in the anesthetized dogs with normal and experimentally reduced renal function. After the administration, furosemide caused diuretic and choleretic response, and was excreted into urine and bile at almost similar rate to plasma concentration decay in normal dogs. Half maximum diuretic response was obtained at 1.5 micrograms/ml of plasma concentration and 100 micrograms/min of urinary excretion rate of furosemide. Acute renal failure was produced in dogs by the intravenous administration of mercuric chloride (HgCl2, 2 mg/kg). In HgCl2-treated dogs, the prolongation of half life (T1/2 beta) and the decrease in plasma clearance were noted with the decreased diuretic response. These changes in parameters appeared to be associated with the decrease in excretion of furosemide into the urine, but not into the bile. Plasma level-diuretic response relationship was extensively shifted to the right in HgCl2-treated dogs, while urinary dose-response relationship did not change significantly between two groups. These results suggest that the decreased response to furosemide in HgCl2-treated dogs seems to be due to the decreased renal clearance rather than to the subsensitivity to furosemide on the site of action.

Acute Kidney Injury↗
PubMed2000

Aerosolized furosemide in the treatment of acute respiratory distress and possible bronchopulmonary dysplasia in preterm neonates.

OBJECTIVE: To review the efficacy and safety of inhaled furosemide in the treatment of acute respiratory distress and possible bronchopulmonary dysplasia (BPD) in preterm neonates receiving ventilator and oxygen support. DATA SOURCES: A MEDLINE search was performed from January 1966 to December 1998 using the key words inhaled or aerosolized furosemide, BPD, preterm, neonate, and infant newborn. STUDY SELECTION AND DATA EXTRACTION: All clinical trials involving the use of inhaled furosemide in ventilator- and oxygen-dependent preterm neonates with acute respiratory distress and possible BPD were evaluated. DATA SYNTHESIS: Inhaled furosemide 1 and 2 mg/kg has improved pulmonary function in preterm neonates without significant adverse effects. However, only a single dose of inhaled furosemide was used in these trials, and pulmonary functions were monitored for only two or four hours after administration. CONCLUSIONS: Inhaled furosemide may be effective, but studies are needed to determine the optimal dosage regimen and long-term risks and benefits of its use in these patients.

Administration, Inhalation↗
PubMed2002

Stability of furosemide in human albumin solution.

OBJECTIVE: To determine the chemical stability of furosemide in human albumin solution over a 28-day period and to assess admixtures for microbiologic contamination. METHODS: Samples were prepared by mixing furosemide injectable solution and 25% human albumin solution in a 1:1 molar ratio. Six bulk containers were prepared and stored in the dark: 3 under refrigeration (approximately 4 degrees C) and 3 at room temperature (approximately 25 degrees C). Study samples were withdrawn from each bulk solution immediately after preparation and at predetermined intervals over the subsequent 28 days. Containers were observed for color change and precipitation against a light and dark background at each sampling interval. Total furosemide concentration was determined using HPLC. Additional vials were prepared and assessed for microbiologic growth at time points corresponding with chemical stability results. RESULTS: A mean of 94.5%+/-1.33% of the initial furosemide concentration remained after 48 hours at room temperature. Under refrigeration, 100.6%+/-1.02% of the initial concentration remained at 14 days. Beyond these respective time points, <90% of the initial furosemide concentration remained. No bacterial or fungal growth was observed. CONCLUSIONS: When combined with 25% human albumin solution and stored under darkness, furosemide is chemically stable and free of microbiologic contamination for 48 hours at room temperature and 14 days under refrigeration.

Albumins↗
PubMed2004

Diuretic effects of subcutaneous furosemide in human volunteers: a randomized pilot study.

BACKGROUND: Furosemide is usually administered by the oral or intravenous route to cardiac patients with hypertension and heart failure, as well as edema. Occasionally, furosemide cannot be administered by these routes. OBJECTIVE: To evaluate the diuretic/natriuretic efficacy of subcutaneously administered furosemide in healthy volunteers. METHODS: This single-center, double-blind, placebo-controlled, randomized, crossover pilot study compared the diuretic effect of subcutaneously administered furosemide and NaCl 0.9% (placebo) in 12 healthy volunteers. The study was conducted over 5 days. Baseline values were determined on day 1. On days 3 and 5, each volunteer was injected with either furosemide 20 mg (2 mL) or 2 mL of placebo subcutaneously. A washout period occurred on day 4. Fluid and dietary intake were controlled on all 3 data collection days. Primary outcome measures consisted of urine volume voided, urine sodium concentration, onset time and volume of initial urine output, and number of voids during 8 hours of urine collection. RESULTS: All outcomes demonstrated statistically significant differences when treatment and placebo groups were compared (p < 0.05). Adverse effects most commonly reported by the participants were minor and included transient burning and stinging at the injection site. CONCLUSIONS: This study demonstrates that subcutaneously administered furosemide is a viable alternative when the oral or intravenous route of administration is not desirable or possible in humans. However, the results of this study need to be corroborated in various patient populations.

Adult↗
PubMed1992

Effect of inhaled furosemide on the bronchial response to lysine-aspirin inhalation in asthmatic subjects.

It has been demonstrated recently that inhaled furosemide inhibits bronchoconstriction induced by cold air, physical exercise, various antigens, and metabisulfite. The goal of the present study was to determine if the inhalation of furosemide would inhibit the bronchoconstriction resulting from the inhalation of lysine-aspirin in aspirin-sensitive asthmatics. Six female subjects with known hypersensitivity to aspirin participated in this crossover study comparing 20 mg of inhaled furosemide and placebo. The volunteers inhaled increasing concentrations of lysine-aspirin after the inhalation of furosemide or placebo. The geometric mean provocative dose causing a 20 percent decrease in the FEV1 (PD20) after the inhalation of placebo was 30.4 mg/ml and the PD20 was equal or below 90 mg/ml in all patients. In contrast, the FEV1 did not decrease by 20 percent in any of the patients pretreated with furosemide when the inhaled concentration was increased to 360 mg/ml. From this study, we conclude that the administration of furosemide blocks the bronchospasm induced by the inhalation of lysine-aspirin in aspirin-sensitive asthmatics.

Administration, Inhalation↗
PubMed1994

Inhaled furosemide is not effective in acute asthma.

As previous studies have suggested that inhaled furosemide may have a protective effect against certain types of provocative challenges in asthmatic subjects, we investigated the role of furosemide in treating acute asthma exacerbations. Twenty-four patients (n = 24) with acute asthma were entered into the study on presenting to the emergency department. They were blindly randomized to receive one of three drug regimens: (1) inhaled furosemide (40 mg) (n = 8); (2) inhaled metaproterenol (15 mg) (n = 7); or (3) the combination of furosemide (40 mg) and metaproterenol (15 mg) (n = 9). We measured FEV1 at entry (time 0) and 15, 30, 45, and 60 min after inhalation of the individual drugs or the combination from a face mask nebulizer. At entry, the three groups did not differ significantly in age (mean +/- SEM = 37.6 +/- 3.6, 38.5 +/- 3.6, and 41.0 years, respectively; p = 0.770), baseline FEV1 (1.01 +/- 0.27, 1.04 +/- 0.27, and 1.25 +/- 0.14 L, respectively; p = 0.620), or theophylline levels (2.87 +/- 1.8, 7.39 +/- 2.8, and 5.29 +/- 2.6 micrograms/ml, respectively; p = 0.498). Pretreatment and posttreatment potassium levels were similar among the three groups. Inhalation of furosemide alone resulted in a 14.9 +/- 10.5 percent change in FEV1 percent from baseline, which was not statistically significant. In contrast, metaproterenol alone resulted in a 42.9 +/- 15.2 percent increase in FEV1 percent (F ratio = 6.226; p = 0.0028). The combination of furosemide and metaproterenol resulted in a change in FEV1 percent that was not statistically different compared with metaproterenol alone (FEV1 percent = 41.9 +/- 12 percent). No significant adverse effects occurred in any of the groups.

Acute Disease↗
PubMed1983

Contributions of central sympathetic neural activity to furosemide-induced increases in plasma renin activity and noradrenaline.

To evaluate the role of the central nervous system on the furosemide-induced increases in plasma noradrenaline (PNA), renin activity (PRA), and aldosterone concentration (PAC), central vasoactive sympathetic structures were inhibited by intravertebral artery infusion of colnidine. Intravertebral artery infusion of clonidine (0.06 microgram/Kg/min) significantly reduced basal PNA, heart rate, and arterial pressure, while both PRA and PAC were increased. Intravenous infusion of the same dose of clonidine caused no significant changes in PNA, PRA, and PAC. Intravertebral artery infusion of clonidine (0.02 or 0.1 microgram/Kg/min) significantly suppressed the furosemide-induced increases in PNA and heart rate, and induced a drop in arterial pressure. Although the furosemide-induced increase in PRA was suppressed by intravertebral artery infusion of clonidine, the furosemide-induced increase in PAC was not affected. These results suggest that the furosemide-induced increase in PNA may be mediated by the central sympathetic nervous system and that some of the furosemide-induced increase in PRA may be mediated by central sympathetic neural activation.

Aldosterone↗
PubMed1987

Cardiac effects of piretanide and furosemide on intact anesthetized dogs and on isolated atria.

The effects of piretanide and furosemide on systemic arterial blood pressure and heart rate were examined in the anesthetized dog and the effects on atrial rate and contractile force were assessed in isolated atrial muscle perfused with heparinized arterial blood from a donor dog. When piretanide was administered intravenously to intact dogs, the depressor and bradycardic responses were produced dose-dependently. There were no significant simultaneous chronotropic or inotropic changes in the isolated atrium. On the other hand, furosemide (1-3 mg/kg) did not induce significant changes in either systemic blood pressure or heart rate in the intact dog. The atrial rate and developed tension were also not affected in the isolated atrium. A potent beta-adrenoceptor blocking agent, propranolol (1 mg/kg i.v.), consistently produced a significant depressor response and a profound negative chronotropic effect in the intact dogs; significant negative chronotropic and inotropic effects were also observed in the isolated atrium. When large doses of piretanide and furosemide were injected intraarterially into the sinus node artery of the isolated atrium, atropine-insensitive negative chronotropic and inotropic effects were induced dose-dependently. The potency of the negative chronotropic effect of piretanide was slightly greater than that of furosemide, but the negative inotropic effect of piretanide was slightly smaller than that of furosemide. These data indicate that piretanide has a depressor effect without significant cardiac influences. However, a high dose of piretanide has negative chronotropic and inotropic effects. These effects were not observed with the doses of furosemide (1-3 mg/kg) employed in this study.

Animals↗
PubMed1998

Acute effects of combined administration of kanamycin and furosemide on the stria vascularis studied by distortion product otoacoustic emission and transmission electron microscopy.

Acute effects of kanamycin and/or furosemide administration on the stria vascularis of the guinea pig cochlea were assessed by distortion product otoacoustic emission (DPOAE) and transmission electron microscopy. Kanamycin alone failed to affect the DPOAE levels and ultrastructural changes. Furosemide alone caused a rapid but reversible fall of the DPOAE levels. No remarkable pathological changes in the strial vascularis were observed after a complete recovery of the DPOAEs. On the other hand, furosemide injection following kanamycin with a 2 hour interval resulted in two patterns of significant changes in the DPOAEs, namely, a sudden drop in the DPOAE levels 2 to 3 hours after furosemide injection and a gradual fall in the DPOAE levels immediately after the incomplete recovery from the furosemide-induced decrease of the DPOAE levels. Ultrastructural changes in the stria vascularis included numerous vacuoles in the strial marginal cells and increased electron density of the intermediate and basal cells. These physiological and morphological changes in the stria vascularis may imply new ototoxic features induced by kanamycin potentiated by furosemide.

Animals↗
PubMed2000

Urinary protein binding does not affect response to furosemide in patients with nephrotic syndrome.

Response to loop diuretics in patients with nephrotic syndrome (NS) is subnormal. Studies in animal models of NS have suggested that binding of diuretic to urinary albumin is one of the mechanisms that may be operative in this diuretic resistance. To explore this hypothesis, 12 patients with NS were studied to determine whether displacement from urinary protein binding with sulfisoxazole would restore response to 120 mg of furosemide. The study was stopped after treating seven patients because it was clear that sulfizoxazole had no effect. Sodium excretion (mean +/- SD) from furosemide alone was 239 +/- 90 versus 240 +/- 115 mEq/8 h with sulfisoxazole. Sulfisoxazole had modest effects on serum pharmacokinetics of furosemide but had no effect on either the time course of furosemide urinary excretion or overall amount excreted: 49 +/- 15 mg versus 54 +/- 12 mg for furosemide alone and furosemide plus sulfisoxazole, respectively. It is concluded that urinary protein binding of loop diuretics is not a major mechanism for the diuretic resistance of NS. In turn, strategies aimed at displacing such binding are unlikely to be clinically helpful.

Adult↗
PubMed2001

Additive effects of a sodium chloride restricted diet and furosemide administration in healthy dogs.

OBJECTIVE: To determine the effects of a low or high sodium (Na) diet with or without furosemide administration on plasma electrolyte concentrations and the renin-angiotensin-aldosterone system in healthy dogs. ANIMALS: 20 healthy adult dogs. PROCEDURE: Dogs were randomly allotted to 4 groups of 5 dogs each as follows: dogs fed a low Na diet (0.08% Na and 0.8% chloride [CI] on a dry matter [DM] basis); dogs fed a low Na diet with added NaCl (1.0% Na and 2.2% Cl on a DM basis); dogs fed a low Na diet and treated with furosemide (2 mg/kg of body weight, PO, q 12 h); and dogs fed a low Na diet with added NaCl and treated with furosemide. Plasma electrolyte concentrations were measured on days 0, 21, and 35. Plasma renin activity and aldosterone concentration were analyzed by use of radioimmunoassays on days 0, 21, 35, and 53. RESULTS: Furosemide treatment significantly decreased plasma Cl concentration and significantly increased plasma renin activity and aldosterone concentration. Dogs fed a low Na diet had significantly higher plasma renin activities and plasma aldosterone concentrations. A significant interaction between a low Na diet and furosemide administration resulted in the lowest plasma Cl concentrations, highest plasma renin activities, and highest plasma aldosterone concentrations. CONCLUSIONS AND CLINICAL RELEVANCE: In healthy dogs, feeding a low Na diet and administering furosemide resulted in an additive effect on plasma Cl concentration, renin activity, and aldosterone concentration, which may be an important consideration for treating dogs with cardiac disease.

Aldosterone↗
PubMed2001

Estimation of the probability for exceeding a threshold concentration of furosemide at various intervals after intravenous administration in horses.

OBJECTIVE: To estimate the probability for exceeding a threshold concentration of furosemide commonly used for regulatory purposes after IV administration of furosemide in horses. ANIMALS: 12 mature healthy horses (6 Thoroughbreds and 6 Quarter Horses). PROCEDURE: Venous blood was collected from each horse prior to and 0.25, 0.5, 0.75, 1, 2, 3, 4, 4.5, 5, and 6 hours after administration of 250 or 500 mg of furosemide. Concentrations of furosemide were determined, using an ELISA. Concentration of furosemide was modeled as a function of time, accounting for inter- and intrahorse variabilities. On the basis of pharmacokinetic data, the probability for exceeding a concentration of 100 ng/ml as a function of time was determined, using a semiparametric smooth functional averaging method. A bootstrap approach was used to assess inherent variation in this estimated probability. RESULTS: The estimated probability of exceeding the threshold of 100 ng of furosemide/ml ranged from 11.6% at 4 hours to 2.2% at 5.5 hours after IV administration of 250 mg of furosemide/horse and 34.2% at 4 hours to 12.3% at 5.5 hours after IV administration of 500 mg of furosemide/horse. The probability of a horse being falsely identified in violation of regulatory concentrations was inversely associated with time and positively associated with dose. CONCLUSIONS AND CLINICAL RELEVANCE: Interhorse variability with respect to pharmacokinetics of furosemide will result in misclassification of some horses as being in violation of regulatory concentrations.

Animals↗
PubMedDate not supplied

Nasal obstruction improvement induced by topical furosemide in subjects affected by perennial nonallergic rhinitis.

Inhaled furosemide decreases bronchial response to several physical and chemical irritants. To evaluate the effect of topical furosemide on nasal resistance in patients affected by perennial nonallergic rhinitis, we studied 12 patients. This diagnosis of perennial nonallergic rhinitis was based on the history of rhinorrhea, sneezing, and nasal obstruction, on anterior rhinoscopy and endoscopy, on negative allergic tests, and on the absence of eosinophilia in nasal secretion. The study was performed on two nonconsecutive days. On the first day, one puff (100 microliters) of 0.9% saline was sprayed into both nostrils and nasal resistance was measured by anterior rhinomanometry before the puff and 15 and 30 minutes later. On the second day, one puff (100 microliters) of a solution of furosemide (10 mg/mL) was sprayed into both nostrils and nasal resistance was measured before the puff and 15, 30, 45, 60, 90, 120, and 180 minutes later. Initial nasal resistance was abnormally high in all patients on both days. A slight but significant increase was observed after spraying isotonic saline (base: 1.38 +/- .69; 15 minutes: 1.47 +/- 0.72; 30 minutes: 1.44 +/- 0.73); by contrast a marked decrease was observed after spraying the furosemide solution. Nasal resistance was lowest between 30 and 90 minutes after giving furosemide. Then it progressively increased, but values at 180 minutes were still lower than the initial ones (base: 1.43 +/- 0.67; 15 minutes: 0.70 +/- 0.47; 30 minutes: 0.48 +/- 0.24; 45 minutes: 0.49 +/- 0.21; 60 minutes: 0.50 +/- 0.20; 90 minutes: 0.56 +/- 0.23; 120 minutes: 0.62 +/- 0.32; 180 minutes: 0.67 +/- 0.30). After topical furosemide, all patients had subjective relief of nasal obstruction that lasted more that 12 hours in 9 subjects.

Administration, Inhalation↗
PubMedDate not supplied

Effect of pre-treatment with inhaled furosemide on allergen nasal challenge.

The inhalation of furosemide has been reported to inhibit the bronchospasm induced by several agents. In the present study, we evaluated the effect of inhaled furosemide on the specific nasal challenge test in patients with allergic rhinitis. A total of 21 consecutive patients with allergic rhinitis (positive skin test and RAST) and a positive basal nasal provocation test (NPT) with the specific allergen were investigated. In each patient, we compared the changes in nasal air-flow (anterior rhinomanometry) during NPT after inhalation of placebo and 20 mg furosemide. The previously positive NPT response to the inhalation of the specific allergen became negative after the furosemide pretreatment in 16 patients (76.2%, p < 0.001, chi-square test). The nasal air flows during NPT were significantly increased after furosemide treatment with respect to placebo inhalation (F = 17.2, d.f. = 1 and 3; p < 0.03; covariance analysis). Our results suggest that the pretreatment with inhaled furosemide in atopic subjects is able to exert a protective effect on the nasal mucosa reactivity to the specific allergen. Therefore, the anti-reactive effect of the drug on the airways is not confined to the bronchial asthmatic response.

Administration, Inhalation↗
PubMed1994

Acute tolerance to furosemide. Pretreatment with captopril or prazosin does not influence diuresis and natriuresis.

To investigate whether the development of acute tolerance to furosemide in human subjects could be prevented or delayed by angiotensin converting enzyme inhibition or alpha 1-receptor blockade, a study was conducted on healthy volunteers. The protocol on the experimental days was identical except for pre-treatment with placebo, captopril or prazosin. During continuous furosemide infusion with urinary furosemide excretion at a constant rate, the subjects became progressively dehydrated, with a maximal decrease in plasma volume of 9-11%. The diuretic/natriuretic response to furosemide was similar in the three protocols. Acute tolerance to diuresis developed earlier than that to natriuresis, again with no differences between the protocols. Not until the plasma volume had decreased by 9% did the natriuresis diminish significantly. In the placebo and captopril protocols acute tolerance was caused mainly by a decreased glomerular filtration rate, and in the prazosin protocol mainly by increased tubular reabsorption. It is concluded that neither ACE inhibition nor alpha 1-receptor blockade prevented or delayed the acute tolerance to furosemide. The results suggest that acute tolerance to furosemide can be induced through different but complementary homeostatic mechanisms in the kidney.

Adult↗