SEARCH · PubMed Health

Results for “FUROSEMIDE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 397 records · Page 22Linked to original sources

PubMed1997

Dilatory effect of furosemide on rat tracheal arterioles and venules.

Furosemide pretreatment greatly reduces the severity of an asthmatic response to several types of bronchoconstrictor challenge. Indirect evidence suggests that furosemide exerts its protective effects by dilating the airway vasculature during thermal stress. To test the hypothesis that furosemide dilates airway microvessels, the tracheas of anesthetized rats were surgically exposed and continuously suffused with Krebs Ringer bicarbonate warmed to 37 degrees C. Tracheal adventitial arterioles (13.0 to 41.0 microns initial diameter, n = 47) and venules (50.0 to 99.0 microns initial diameter, n = 46) were visualized with a videomicroscope, and vessel diameters were measured using videocalipers. When vessels were preconstricted with 10(-4) M phenylephrine, a selective alpha 1-adrenergic agonist, and then treated with 10(-4) M furosemide, significant (p < 0.05) dilation was observed in both arterioles (from 64.6 to 79.5% of their initial diameter) and venules (from 52.1 to 65.4% of their initial diameter). When vessels were preconstricted with 10(-4) phenylephrine, after pretreatment with the cyclooxygenase inhibitor indomethacin (5.0 mg/kg), 10(-4) M furosemide significantly dilated arterioles (from 77.5 to 93.0% of their initial diameter) and venules (from 58.5 to 80.1% of their initial diameter). In vessels preconstricted with 10(-3) M L-NAME, an inhibitor of nitric oxide synthesis, addition of 10(-4) M furosemide to the suffusion still caused significant dilation in arterioles, from 77.4 to 88.8% of their initial diameter, and in venules from 79.5 to 86.7% of their initial diameter. These data confirm that furosemide, when applied topically, dilates tracheal arterioles and venules by cyclooxygenase- and nitric oxide-independent mechanisms.

Animals↗

PubMed2000

Inhaled furosemide greatly alleviates the sensation of experimentally induced dyspnea.

Furosemide is known to influence the activity of vagally mediated mechanoreceptors in the airways. Because vagal afferent fibers may play an important role in modulation of the sensation of dyspnea, it is possible that inhaled furosemide may modify the sensation of dyspnea. In a double-blind, randomized, crossover study, we compared the effect of inhaled furosemide on dyspneic sensation with that of placebo. Severe dyspneic sensation was induced in 12 healthy subjects in two ways: (1) breathholding and (2) loaded breathing with a combination of inspiratory resistive load (240 cm H(2)O/L/s) and hypercapnia induced by extra mechanical dead space (0.26 L). Subjects were asked to rate their sensation of respiratory discomfort using a visual analogue scale (dyspneic VAS). Breathholding times and changes in dyspneic VAS score during a 5-min period of loaded breathing were measured after inhalation of placebo and furosemide (40 mg). Total breathholding time after inhalation of furosemide (median, 93 [interquartile range, 78 to 112]s) was prolonged compared with the total breathholding time after placebo inhalation (67 [47-74]s). We also found that respiratory discomfort during loaded breathing after inhalation of furosemide develops more slowly and is less than that observed after inhalation of placebo. Our findings indicate that inhaled furosemide greatly alleviates the sensation of dyspnea induced experimentally by breathholding and by a combination of resistive loading and hypercapnia.

Administration, Inhalation↗

PubMed2004

Effects of inhaled furosemide on exertional dyspnea in chronic obstructive pulmonary disease.

The aim of this study is to investigate the effects of inhaled furosemide on the sensation of dyspnea produced during exercise in patients with stable chronic obstructive pulmonary disease (COPD). In a double-blind, randomized, crossover study we compared the effect of inhaled furosemide on dyspneic sensation during exercise testing with that of placebo. Spirometry and incremental and constant-load exercise testing were performed after inhalation of placebo or furosemide on 2 separate days in 19 patients with moderate or severe COPD. Subjects were asked to rate their sensation of respiratory discomfort using a 100-mm visual analog scale. There was significant improvement in mean FEV1 and FVC after inhalation of furosemide (p = 0.038 and 0.005, respectively) but not after placebo. At standardized exercise time during constant-load exercise testing but not during incremental exercise, the mean dyspneic visual analog scale score was lower after inhalation of furosemide compared with placebo (33.7 +/- 25.2 vs. 42.4 +/- 24.0 mm, respectively, p = 0.014). We conclude that inhalation of furosemide alleviates the sensation of dyspnea induced by constant-load exercise testing in patients with COPD and that there is significant bronchodilation after inhalation of furosemide compared with placebo in these patients.

Administration, Inhalation↗

PubMed2004

Effects of acute hypovolaemia by furosemide on tracheal transepithelial potential difference and mucus in dogs.

Furosemide is a potent diuretic that affects water transfer across the respiratory epithelium, which is closely related to the transepithelial potential difference (PD). Water is a critical factor that determines mucus transport; an important lung defence mechanism that removes particles and microorganisms from the respiratory system. The aim of the present study was to investigate the acute effects of furosemide and hypovolaemia on tracheal PD and mucus properties. A total of 36 male mixed-breed dogs were submitted to anaesthesia, mechanical ventilation and haemodynamic monitoring. They were randomly assigned to three groups consisting of: a control group, a furosemide (40 mg i.v.) + hypovolaemia group, and a furosemide (40 mg i.v.) + volume replacement group. Tracheal PD and mucus samples were collected at time 0, 1 and 2 h after intervention. Mucus properties were analysed by means of a magnetic microrheometer and in vitro mucociliary transportability on the frog palate. Compared to controls, furosemide decreased PD to intermediate values, and only significantly when associated with hypovolaemia (-13+/-5 and -8+/-2 mV, time 0 and 2 h, respectively). In addition to the direct effect of furosemide, these results indicate that hypovolaemia also affects ion transport in the tracheal membrane. Furosemide and hypovolemia have no acute effects on respiratory mucus properties.

Acute Disease↗

PubMed1998

Furosemide inhibits 11beta-hydroxysteroid dehydrogenase type 2.

11Beta-hydroxsteroid dehydrogenase 2 (11beta-OHSD2) protects the nonselective renal mineralocorticoid receptor from the endogenous glucocorticoid cortisol. Thus, drugs inhibiting 11beta-OHSD2 might enhance urinary loss of potassium. As diuretics influence the renal handling of potassium, we analyzed the impact of 13 commonly used diuretics on 11beta-OHSD2. Furosemide was the only inhibitor. Its inhibition constant (Ki) was 30 micromol when extracts from COS-1 cells transfected with human 11beta-OHSD2 were used as an enzyme source. The type of inhibition was competitive. To establish whether furosemide inhibits 11beta-OHSD2 and 11beta-OHSD1 in the renal target tissue, isolated tubular segments from rats were analyzed. Furosemide decreased the oxidative activity of 11beta-OHSD2 in intact distal tubules and 11beta-OHSD1 in proximal convoluted tubules. For the assessment of furosemide on the excretion of corticosterone metabolites in vivo, rats were given furosemide i.p., and the ratio of tetrahydrocorticosterone plus 5alpha-tetrahydrocorticosterone to 11-dehydrotetrahydrocorticosterone was determined in urine. This ratio increased after the administration of furosemide in all animals, indicating inhibition of the oxidative activity of 11beta-OHSD. Thus, furosemide inhibits the 11beta-OHSD2 enzyme in the target tissue and might by that mechanism enhance the mineralocorticoid effect of 11beta-hydroxyglucocorticoids.

11-beta-Hydroxysteroid Dehydrogenases↗

PubMed1988

Increased diuretic response to furosemide in rats with glycerol-induced acute renal failure.

To clarify the diuretic response to furosemide in a diseased state, the urinary excretion of furosemide, water, and electrolytes was examined after a single intravenous injection of furosemide in control rats and rats with mild acute renal failure (ARF) induced by glycerol. The urinary recovery of furosemide was similar in the control and ARF rats. However, the diuretic response to furosemide was increased in ARF rats compared with control rats. Although the relationship between the urine flow rate (UFR) and the urinary excretion rate of (Na+ + K+) (UV Na + K) was the same in both groups, the urinary excretion rate of K+ (UV K) was decreased in ARF rats. The concentrating ability in ARF rats was also decreased compared with that in control rats. By infusion of aldosterone in ARF rats, both UV K and the concentrating ability were increased and the diuretic response to furosemide was decreased, whereas the relationship between UFR and UV Na + K was not changed. Therefore, it is concluded that the increased diuretic response to urinary excretion of furosemide in ARF rats may be caused, at least in part, by the decreased concentrating ability along the nephron.

Acute Kidney Injury↗

PubMed1982

Effect of furosemide on plasma clearance, anticoagulant effect and protein binding of warfarin in rats.

The effect of furosemide on the elimination, anticoagulant effect and the in vitro and in vivo protein bindings of warfarin was examined in rats. The pharmacokinetic parameters of warfarin and prothrombin complex activity (PCA) after a single i.v. coadministration with warfarin (1.2 mg/kg) and furosemide (1.67 mg/kg) were not significantly different as compared with those in the group injected warfarin alone; however when coadministered with 5 mg/kg of furosemide, the elimination rate constant was significantly increased and PCA was markedly enhanced beyond 60 h after administration. The concurrent treatment with warfarin and a higher dose (10 mg/kg) of furosemide caused an increase in the anticoagulant effect of warfarin even at earlier periods after administration. Both the unbound warfarin concentration in serum at 30 min and the amount of warfarin extracted into liver at 2 h after a single i.v. dosing in the coadministered group were significantly increased as compared with those in the group received warfarin alone. Results from in vitro binding studies using bovine serum albumin and rat plasma showed a typical competitive nature of protein binding of warfarin and furosemide at the same binding sites. These results suggest that the interactions, such as the displacement of warfarin binding at albumin binding sites, between warfarin and furosemide are produced, when a high dose of furosemide was coadministered.

Administration, Oral↗

PubMed1986

Effect of furosemide and trimethazidine on kinetic behavior and hypotensive effect of hydralazine in rats.

The pharmacokinetic and pharmacodynamic interactions between hydralazine (HP) and furosemide or trimethazidine were determined following single i.v. and repeated (7 d) oral administrations in rats. Both furosemide and trimethazidine caused a significant decrease in the level of plasma protein binding of HP in vivo after i.v. administration. However, in vitro there was no effect on binding. Coadministration of HP and furosemide at lower doses (1.67 mg/kg, i.v. and 5 mg/kg, oral) reduced the hypotensive effect, accompanying the enhanced elimination of HP from plasma after a single i.v. and repeated oral treatment when compared to the result obtained with HP alone. The elimination of HP accelerated by the lower doses of furosemide may be probably due to the increase in renal clearance by the diuretic effect of furosemide. On the contrary, a high dose (10 mg/kg, i.v.) of furosemide temporarily strengthened the hypotensive effect, probably due to the additional hypotensive action of furosemide itself. Trimethazidine (0.75 and 3.75 mg/kg) gave a small increase in the hypotensive effect of HP in spite of the partially enhanced clearance of HP. The pharmacodynamic analysis showed that the hypotensive effect of HP depended upon the plasma HP concentration in each treatment, although the response curves of HP were partly altered by the combined drugs. The present study also suggests a validity of co-administration of HP and diuretics for the therapy of hypertension and heart failure.

Animals↗

PubMed1992

Chronopharmacology of furosemide in rats with amikacin-induced acute renal damage.

To examine the influence of amikacin-induced acute renal damage on the urinary excretion of furosemide and the time-dependent variation in the urinary amount of the agent, amikacin (1.2 g/kg) was given intraperitoneally to Wistar rats. Study I: Three percent b.w. of 1% NaCl solution was given orally before and after amikacin treatment, and an 8-hour urine for N-acetyl-beta-D-glucosaminidase (NAG) was collected. Study II: Furosemide (30 mg/kg) in 3% b.w. of 1% NaCl solution was given orally at 12 a.m. or 12 p.m. before and after amikacin treatment, and an 8-hour urine for sodium and furosemide was collected. Following amikacin treatment, urinary excretion of NAG increased, while urine volume and urinary excretion of sodium and furosemide decreased. Urinary excretion of furosemide and its diuretic effects were significantly greater at 12 a.m. than at 12 p.m. before and after treatment. However the time-dependent differences in these parameters were diminished by amikacin treatment. These results suggest that the urinary excretion of furosemide is reduced and the extents of the time-dependent variation in the urinary furosemide and its diuretic effects are altered in rats with amikacin-induced renal damage.

Acetylglucosamine↗

PubMed2000

Involvement of the renal kallikrein-kinin system in furosemide-induced natriuresis in rats.

This study examined whether the renal kallikrein-kinin system (KKS) is involved with furosemide-induced natriuresis in rats. Intravenous administration of furosemide (10 mg/kg) to anesthetized rats infused with physiological saline (saline) increased renal KK excretion as well as urine volume and urinary excretions of sodium, chloride and potassium. The change in the increase of renal KK excretion by furosemide at a dose of 1.0 mg/kg relative to the control was larger than that of urine volume. Pretreatment with a B2-receptor antagonist, 8-[3-[N-[(E)-3-(6-acetamidopyridin-3-yl)acryloylglycyl]-N-methylamino]-2,6-dichlorobenzyloxy]-2-methylquinoline (FR173657, 100 mg/kg), significantly inhibited the furosemide-induced natriuresis by 58.6%. The effect of FR173657 on the furosemide-induced natriuresis was also examined in hypotonic saline-loading rats. Similar to the saline-loading rats, urinary excretion of sodium collected during the first 8 h in metabolic cages significantly reduced by 22.4% when FR173657 (100 mg/kg) was given concurrently with furosemide (100 mg/kg) and hypotonic saline (5% of body wt.). These results indicate that furosemide increased renal KK excretion through a mechanism different from a washout mechanism and induced natriuresis partly through an augmentation of the renal KKS following the increase in renal KK excretion in both the saline- and hypotonic saline-loading rats.

Animals↗

PubMed2002

Discontinuation of furosemide decreases PaCO(2) in patients with COPD.

STUDY OBJECTIVE: To evaluate whether the discontinuation of furosemide treatment resulted in a decrease in PaCO(2) and an increase in daytime and nocturnal oxygenation. BACKGROUND: Furosemide is widely prescribed in patients with COPD for the treatment of peripheral edema. It is known that furosemide causes a metabolic alkalosis. A diminished chemoreceptor stimulation may cause a decreased alveolar ventilation. DESIGN: Randomized, double-blind, placebo-controlled, crossover trial. SETTING: Department of Pulmonology, Rijnstate Hospital Arnhem, the Netherlands. PATIENTS: Twenty patients with stable COPD (10 men; median age, 70 years [range, 58 to 81 years]; FEV(1) 35% predicted [range, 19 to 70% predicted]). Subjects were included if they had received furosemide, 40 mg/d, for the treatment of peripheral edema for at least a month and if they had a mean nocturnal arterial oxygen saturation (SaO(2)) < 92%. Patients with cardiac left and/or right ventricular dysfunction, sleep apneas, and patients receiving other diuretics, angiotensin-converting enzyme inhibitors, potassium or chloride replacement therapy, or long-term oxygen treatment were excluded. INTERVENTION: Furosemide was discontinued for 1 week and replaced by placebo treatment in the first or the second week. MEASUREMENTS AND RESULTS: Ventilation, daytime arterial blood gas levels, and nocturnal SaO(2) were measured at baseline, after 1, and after 2 weeks. Sixteen subjects completed the study. Ventilation increased from 10.4 L/min (range, 6.7 to 15.4 L/min) at baseline to 11.6 L/min (range, 8.7 to 14.0 L/min) after discontinuation of furosemide (p < 0.05). PaCO(2) decreased from 45 mm Hg (range, 35 to 64 mm Hg) to 41 mm Hg (range, 32 to 61 mm Hg; p < 0.01). Daytime and nocturnal oxygenation did not improve. CONCLUSIONS: Although it does not improve oxygenation, the discontinuation of furosemide decreases PaCO(2) in patients with COPD.

Aged↗

PubMed1982

Potentiation of toxicity and positive inotropic effect of ouabain by furosemide in guinea pig heart.

The present study was undertaken to elucidate the potentiation by furosemide of toxicity and positive inotropic effect of ouabain in guinea pigs. Arrhythmogenic responses to ouabain as well as the lowering of its lethal dose were potentiated by pretreatment with furosemide in guinea pigs. The potentiation of ouabain toxicity after furosemide administration was inhibited by pretreatment with potassium sparing diuretic, prorenoate. Furosemide-induced potentiations of contractile force and arrhythmogenic effect of ouabain were also observed in isolated guinea pig papillary muscle. However after pretreatment with furosemide, ouabain produced arrhythmias without any significant changes in either left ventricular or subcellular fractions binding of 3H-ouabain in guinea pigs. These findings suggest that furosemide-induced potentiation of ouabain toxicity is at least in part associated with the decreased intracellular potassium content of guinea pig heart. It was also demonstrated that the positive inotropic action induced by subtoxic dose of ouabain was potentiated by furosemide in guinea pig papillary muscle preparation.

Animals↗

PubMed2003

Lowering of furosemide dosage after clinical stabilization in patients with congestive heart failure.

OBJECTIVES: This study was performed to examine the safety of reducing the long-term doses of furosemide administered to patients with congestive heart failure (CHF) stabilized on a standard medical treatment. METHODS AND RESULTS: Twenty-nine patients with advanced CHF were treated with enalapril, digoxin, nitrates, and furosemide, as needed to alleviate their symptoms, and remained clinically stable for at least 3 months on those doses. Subsequently, the daily dose of furosemide was reduced to 1/3 of the previous dose, while the concomitant therapy was unchanged. All patients underwent a thorough clinical evaluation and right-heart catheterization before and 2 months after the furosemide dose reduction. After the treatment optimization the NYHA functional class decreased from 2.3 +/- 0.6 to 1.4 +/- 0.6 (p = 0.000), and the left ventricular ejection fraction increased from 22 +/- 10% to 32 +/- 13%, (p = 0.000). Clinical and haemodynamic evaluation before and after 2 months of treatment with lower furosemide doses showed that 24 of the 29 patients (83%) remained in a stable NYHA functional class and maintained a stable haemodynamic status. In the remaining 5 patients (17%), mean NYHA functional class increased from 1.8 +/- 0.4 to 2.4 +/- 0.6 (p = 0.07), accompanied by a significant increase of the right and left ventricular filling pressures from 4.2 +/- 2.7 to 9.0 +/- 3.0 mm Hg, p = 0.018 and from 8.6 +/- 3.0 to 19.8 +/- 3.6 mm Hg, p = 0.017, respectively. These 5 patients returned to a stable clinical status upon resumption of the prior doses of furosemide. CONCLUSIONS: Most patients with chronic CHF who were clinically stabilized on high doses of furosemide remained stable on a maintenance dose equal to one-third of the dose needed for their stabilization. Patients unable to tolerate the dose reduction regained their previous clinical status following the resumption of the prior diuretic doses.

Adult↗

PubMedDate not supplied

Effect of glycerol on the EP decrease caused by furosemide.

A change in endocochlear potential (EP) following furosemide injection was observed in regard to prior glycerol administration in two groups of guinea pigs. In one group, various doses of furosemide (20, 30, 40, 50 mg/kg) were injected, while in the other, glycerol (50 v/v %, 1 ml/kg) was injected prior to the furosemide (20, 30, 40 mg/kg) injection. In the glycerol-furosemide group, the decrease in EP was 40% greater than in the furosemide group. Therefore, glycerol was thought to potentiate the EP lowering action of furosemide. Such an effect of glycerol was assumed to be resulted by facilitating the access of furosemide to the site of action in the stria vascularis.

Action Potentials↗

PubMed1988

Delayed tolerance to furosemide diuresis. Influence of angiotensin converting enzyme inhibition by lisinopril.

The role of the renin-angiotensin-aldosterone system in the development of tolerance to the diuretic effect of furosemide was investigated in 12 healthy male volunteers. Furosemide in a dose of 40 mg daily for one week had a brisk acute diuretic effect, but did not lead to dehydration, hyponatremia or fall in blood pressure. The reason for this was a reduction in sodium excretion between doses (rebound effect) and a decrease in sensitivity to furosemide from day 1 to day 7. The latter phenomenon is referred to as delayed tolerance to furosemide. Inhibition of angiotensin converting enzyme with lisinopril 20 mg daily did not change the renal furosemide excretion rate, the renal sensitivity to furosemide or the tolerance development. Thus, delayed tolerance to furosemide diuresis was not related to dehydration or activation of the renin-angiotensin-aldosterone system. Other mechanisms, probably intrarenal, will have to be looked for.

Adult↗

PubMed1997

Furosemide given by inhalation ameliorates acute exacerbation of asthma.

Previous studies have suggested that inhaled furosemide may have a protective effect against a wide variety of bronchoconstrictor agents, but a therapeutic effect has not been established in acute exacerbation of asthma. The purpose of this study was to investigate whether inhaled furosemide would exhibit any therapeutic benefit in acute asthma. We conducted a double-blind, placebo-controlled, randomized study in 40 patients with acute mild or moderate exacerbation of asthma. All patients received intravenous (i.v.) aminophylline 250 mg for 90 min and i.v. hydrocortisone 100 mg at entry. After randomization, 3 patients were excluded from the final analysis. At 30 min after starting i.v. aminophylline, 20 patients were given inhaled furosemide 20 mg and 17 patients received normal saline as placebo-control. Both inhalations were given by a jet nebulizer. The baseline forced expiratory volume at 1 sec (FEV1), peak expiratory flow rate (PEFR), and serum concentration of theophylline did not differ between the two groups. An increase in FEV1 in the furosemide group by 28.2 +/- 5.9% (mean +/- SE) was noted at 60 min, and this was significantly higher than in the control group. PEFR at 60 min was also significantly higher in the furosemide group than in control group. We conclude that inhaled furosemide has a bronchodilator effect on mild to moderate exacerbation of asthma when it is used with i.v. theophylline. Inhaled furosemide may benefit certain acute asthma patients, especially those suffering complications from the adverse effects of beta 2-agonists.

Acute Disease↗

PubMed1998

Effect of chronic furosemide administration on acid-base balance in patients with chronic hypercapnic respiratory failure.

We quantitatively analyzed the effect of long-term administration of oral furosemide on the PaCO2 - H+ relationship in patients with chronic hypercapnic respiratory failure. In this study we measured arterial blood gases of eighteen outpatients (mean duration of visits, 7.6 years; mean rise of PaCO2, 15.4 mmHg). We obtained linear regression lines for PaCO2 - H+, and determined their Y-axis intercepts and slopes. The results indicated that an increase in the administered dose of furosemide decreased linearly the Y-axis intercept of the regression line [(Y-intercept) = - 6.9(dose of furosemide) + 30.9, r = 0.81], and increased linearly the slope of the regression line [(slope) = 0.094(dose of furosemide) + 0.22, r = 0.74]. Thus, the regression line of the PaCO2 - H+ relationship moved downward and became steeper at higher doses of furosemide. The regression lines for each dose of furosemide crossed at a PaCO2 of 75 mmHg. We concluded that there is a mutual interaction between the renal and respiratory mechanisms for acid-base balance in chronic hypercapnia and the effect of furosemide on the PaCO2 - H+ relationship is negligible in severe hypercapnia.

Acid-Base Equilibrium↗

PubMed1998

Comparison of therapies with torasemide or furosemide in patients with congestive heart failure from a pharmacoeconomic viewpoint.

This observational study compared patients suffering from congestive heart failure (CHF) who were treated with loop diuretics torasemide or furosemide. Data documenting the course of the disease and its associated costs over a period of one year were collected retrospectively. A total of 400 CHF patients, 200 in each treatment group, were included in the analysis. Concomitant ACE inhibitor therapy was received by 46% of patients in both groups. More torasemide-treated patients (38.0%) than furosemide-treated patients (24.5%) achieved an improvement in NYHA class in the one-year period. The main difference between the two groups was the number of CHF-related hospitalisations: 62 vs 324 hospital days due to CHF were necessary among torasemide- and furosemide-treated patients, respectively. Thus torasemide treatment was associated with an 80% reduction in hospital days compared with furosemide. Furthermore, about 30% fewer working days were lost in the torasemide group than in the furosemide group (441 days vs 617 days, respectively). Direct and indirect costs were evaluated, resulting in overall annual costs of DEM 1502 per torasemide-treated patient and DEM 1863 per furosemide-treated patient. A cost-effectiveness analysis showed a difference between the therapies of DEM 3651 in favour of torasemide. In conclusion, treatment with torasemide improved clinical outcome and was more cost-effective than with furosemide.

Adult↗