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PubMed1977

Effects of furosemide on glomerular filtration rate and clearance of practolol, digoxin, cephaloridine, and gentamicin.

Furosemide was shown to decrease inulin clearance in 20 of 27 normal subjects. The depression in inulin clearance occurred in both water-loaded and non-water-loaded subjects. The renal clearance of practolol, but not digoxin, was reduced when furosemide was given. The average total plasma clearances of gentamicin and of cephaloridine over a 6-hr period were decreased after furosemide. The reduced clearances of the antibiotics were associated with higher plasma levels, the increase in antibiotic concentration being as much as 100% at 1 hr after an intravenous bolus injection.

Adult↗
PubMedDate not supplied

Effect of intravenous furosemide on the renal excretion of digoxin.

The effect of an 80-mg intravenous dose of furosemide on the urinary excretion of digoxin was determined in three adult men with normal renal function, each of whom was taking 0.25 mg digoxin daily on a chronic basis. On two separate days, serum samples were taken and urine was collected every 2 hours over an 8-hour period for determination of digoxin, creatinine, calcium, and sodium concentrations. On the first day of study, a saline bolus was given intravenously, and on the second day, furosemide was given. In all subjects, urinary digoxin excretion increased after furosemide in direct proportion to the increase in urine volume. No consistent correlation was seen between digoxin excretion and creatinine, calcium, or sodium output. No significant changes in serum digoxin were found in this active study. These results are consistent with the hypothesis that increasing glomerular filtration rate or total urine volume increases the renal excretion of digoxin and may result in increased total urinary output of this glycoside.

Calcium↗
PubMedDate not supplied

High-dose furosemide in Nigerians with severe chronic renal failure: effect on fecal water content.

The effect of high doses of furosemide, 200 to 800 mg daily, has been studied in 12 Nigerias with edema associated with severe chronic renal failure and hypertension. They all responded well and lost their edema fluid during a period which varied from 10 to 57 days. The fecal water content and the frequency of bowel opening while on furosemide were significantly higher than without furosemide in six of these patients. It is concluded that the gastrointestinal tract is a major contributory site of fluid loss in patients with grossly impaired renal function.

Adolescent↗
PubMedDate not supplied

Comparison of adverse reactions to bumetanide and furosemide.

In 58 clinical studies, adverse reactions to bumetanide were evaluated in 493 patients and compared with those in 220 patients treated with furosemide. The comparison diuretics were administered to patients with edema secondary to congestive heart failure, and renal and hepatic disease. In addition to observation of clinical variables, laboratory tests were done to evaluate the effects of the diuretics on serum electrolyte levels. The results indicate that bumetanide, as furosemide, is an effective diuretic free of significant adverse effects when administered in doses within the recommended therapeutic dose range. Audiometric studies suggest that bumetanide is possibly safer than furosemide with regard to ototoxicity.

Breast↗
PubMedDate not supplied

Comparative efficacy and safety of bumetanide and furosemide in long-term treatment of edema due to congestive heart failure.

Bumetanide and furosemide were compared for efficacy in reducing edema due to congestive heart failure in 28 patients (21 receiving bumetanide and seven receiving furosemide) in a long-term study for periods from one week to 18 months. In both groups the patients showed decreases in body weight, abdominal girth, edema, hepatomegaly, blood pressure, and heart rate. Commonly observed decreases frequently achieved statistical significance, more often with bumetanide, but the differences between treatments were rarely statistically significant. Both drugs were generally well tolerated. A breast nodule and gynecomastia were each reported once in the bumetanide group as was gynecomastia in one patient who had been on furosemide, all remotely related to test drugs. Soft stools, flatulence, mild constipation, and diminished vision each reported once in the bumetanide group were judged to be unrelated or remotely related to the drug therapy. Tendencies toward hypokalemia, hypochloremia, alkalosis, and hyperuricemia without clinical gout were deemed the result of the pharmacologic action of the diuretics. Others were attributable to the underlying disease state of these patients. Both diuretics proved to be effective in the treatment of cardiac edema and other manifestations of heart failure. Bumetanide treatment beyond six months in 11 patients indicated continued safety as well as efficacy.

Aged↗
PubMedDate not supplied

Effect of furosemide on the pharmacokinetics of gentamicin in patients.

The clearances of inulin and gentamicin were studied before and after intravenous furosemide in seven patients. There was a significant fall in glomerular filtration rate after furosemide and a similar though less marked fall in gentamicin clearance in six of the seven subjects. Small but consistent increases in plasma gentamicin concentrations were observed after furosemide. The reduction in clearance may explain the enhanced risk of nephrotoxicity in patients receiving both aminoglycosides and diuretics.

Aged↗
PubMedDate not supplied

Furosemide vasodilates the canine gastrointestinal tract.

The ability of furosemide to induce vasodilation in the canine gastrointestinal system was studied by quantitative flowmetry. Blood flow and conductance increased maximally by 60 per cent in the stomach and duodenum and by 80 per cent in the small and large intestine. Vasodilation was evident at 2.4 mg/kg furosemide and higher. The onset of vasodilation occurred at 24 to 30 seconds and was maximal at 36 seconds in the stomach, at 66 seconds in the duodenum, at 78 to 84 seconds in the small intestine, and at 90 seconds in the large intestine. Hepatic arterial, splenic, and renal blood flows were unchanged. Simultaneous arteriovenous sampling from the small intestine indicated that the increased blood flow was not associated with increased O2 consumption. However, CO2 addition to the venous effluent decreased by 70 per cent. These data indicate that furosemide has a vasodilatory action on the gastrointestinal tract due either to a delayed effect on the vascular smooth muscle cell or on anaerobic bowel wall metabolism. The CO2 data are compatible with, but do not prove, stimulation of secretion of HCO3- by the intestinal mucosa.

Animals↗
PubMed1994

Bumetanide and furosemide inhibited vascular endothelial cell proliferation.

In this study, we examined the role of the bumetanide-sensitive Na+/K+/Cl-cotransport in the mitogenic signal of vascular endothelial cell proliferation. The activity of the Na+/K+/Cl- cotransport is dramatically decreased in quiescent subconfluent cells, as compared to subconfluent cells growing in the presence of FGF. The Na+/K+/Cl- cotransport activity of quiescent subconfluent cultures deprived of FGF decreased to 6%, whereas that of quiescent cells grown to confluency was reduced to only 33% of the activity of subconfluent cells growing in the presence of FGF. The basal low activity of Na+/K+/Cl- cotransport in the quiescent subconfluent vascular endothelial cells was dramatically stimulated by FGF. In order to explore the role of the Na+/K+/Cl- cotransport in the mitogenic signal of the endothelial cells, the effect of two specific inhibitors of the cotransport -furosemide and -bumetanide was tested on cell proliferation induced by FGF. Bumetanide and furosemide inhibited synchronized cell proliferation measured by direct counting of cells and by DNA synthesis. Inhibition by furosemide and bumetanide was reversible; removal of these compounds completely released the cells to proliferate. These results indicate that the effect of these drugs is specific and is not due to an indirect toxic effect. This study clearly demonstrates that the FGF-induced activation of the Na+/K+/Cl- cotransport plays a role in the mitogenic signal pathway of vascular endothelial cells.

Animals↗
PubMed2004

Evaluation of the reproducibility of intrarenal R2* and DeltaR2* measurements following administration of furosemide and during waterload.

PURPOSE: To estimate the reproducibility of BOLD MRI measurements in the evaluation of intrarenal oxygenation levels. MATERIALS AND METHODS: In this study, the reproducibility of semiquantitative BOLD MRI measurements performed on a 1.5 T scanner with a multiple gradient-echo sequence in the renal medulla and cortex, and their response to furosemide and waterload, were assessed in eight healthy young subjects (25.6 +/- 4.1 years). Each subject underwent an identical experimental procedure on two separate days. RESULTS: Renal R2* measurements were shown to be reproducible within approximately 12% from day to day based on a coefficient of variance (CV) analysis. The changes in R2* (DeltaR2*) following administration of furosemide were statistically significant, as shown by ANOVA and a paired Student's t-test, and were deemed reliable based on the reliable change index (RCI). However, DeltaR2* values following waterload were not statistically significant, and were not deemed reliable. CONCLUSION: R2* measurements were reproducible over 270 days within 12%. Furosemide produced a significant and reliable change (approximately 30%), and the magnitude of change (5.7 s(-1)) was reproducible and consistent with our previous data. The response to waterload, however, did not reach statistical significance, and the magnitude did not reach the level that we had previously reported.

Adult↗
PubMed1976

Absorption, distribution, metabolism, and excretion of furosemide in dogs and monkeys I: analytical methodology, metabolism, and urinary excretion.

35S-Furosemide was administered to beagle dogs and rhesus monkeys in an oral solution on a single and a 20 repeated 5-mg/kg/day dosing regimen. Following the single dose, 25.0% (dogs) and 24.0% (monkeys) of the dose were excreted in the urine in 24 hr. TLC analysis demonstrated that both species had similar excretory patterns; i.e., over 80% of the amount excreted in the urine was present as unchanged durosemide and the remainder was composed of a known metabolite, saluamine, and an as yet unidentified metabolite(s). The repetitive dosing regimen did not appear to alter significantly either the total amount recovered in the 24-hr urine or the excretion pattern. Studies in dogs showed that only 50-60% of furosemide was absorbed from oral solution. A significant biliary secretion elimination pathway for furosemide also was observed.

Animals↗
PubMed1994

Development and evaluation of a monolithic floating dosage form for furosemide.

The poor bioavailability of orally dosed furosemide (60%), a weakly acidic drug, is due to the presence of a biological window comprised of the upper gastrointestinal tract. The purpose of the present study was to develop and optimize in vitro a monolithic modified-release dosage form (MMR) for furosemide with increased gastric residence time and to evaluate the in vivo performance of the dosage form. The principle of floatation was used to restrict the MMR to the stomach. A two-factor three-level full factorial experimental design was employed for formulation development. A flow-through cell was designed to evaluate in vitro dissolution parameters. Quadratic regression models indicated the polymer viscosity and polymer:drug ratio to be significant (p < 0.05) formulation factors in determining the duration of buoyancy and the release profile. Statistical optimization using response surface methodology with certain physiological constraints relating to gastric emptying time predicted an optimal MMR. In vivo evaluation of the optimized MMR in beagle dogs resulted in a significant increase (p < 0.05) in the absolute bioavailability for the MMR dosage form (42.9%) as compared to the commercially available tablet (33.4%) and enteric product (29.5%). Significant in vitro/in vivo correlations (p < 0.05) were obtained for the MMR using deconvolution analysis normalized for bioavailability. The floating dosage form was found to be a feasible approach in delivering furosemide to the upper gastrointestinal tract to maximize drug absorption.

Animals↗
PubMed2002

Modification of ureteral motility and promotion of urine flow around an intraureteral obstruction by CL-316243, phenylephrine, and furosemide in dogs.

The aim of this study was to evaluate the effects of a beta3-adrenoceptor (AR) agonist (CL-316243), an alpha1-AR agonist (phenylephrine), and a loop diuretic (furosemide) on the spontaneous rhythmic contractions of the isolated canine ureter and on an acute ureteral obstruction produced by inflation of a balloon catheter in anesthetized dogs. In the isolated ureter, CL-316243 concentration dependently reduced both the amplitude and frequency of the rhythmic contractions (pD(2): 7.19 +/- 0.33), whereas phenylephrine significantly enhanced both variables (pD(2): 5.26 +/- 0.09) and furosemide reduced them only slightly. In the acute ureteral obstruction model, the intraureteral pressure (IUP) gradually rose to reach a plateau of 58.9 mm Hg after inflation of a balloon catheter within the lower ureter. Intravenous administration of CL-316243 (0.3 microg/kg) significantly reduced the elevated IUP and the resumed urine flow (UF), leading to a sustained reduction in the IUP. In contrast, the IUP continued to increase above the plateau level for 10 minutes after phenylephrine administration (10 microg/kg) and for 30 minutes after furosemide administration (1,000 microg/kg). In the phenylephrine group, the UF resumed when the IUP reached 75.8 mm Hg, and thereafter the IUP gradually decreased in parallel with the increase in the UF. From these results, we conclude that in dogs, CL-316243 reduces the IUP by allowing the UF to resume as a result of a relaxation of ureter at the obstruction site, whereas with phenylephrine, the reduction in the IUP is secondary to a resumption in the UF resulting from an induced contraction of ureter that causes an increase in hydrostatic pressure above the obstruction site.

Adrenergic alpha-Agonists↗
PubMed1981

Furosemide induced hepatotoxicity.

Furosemide-induced (400mg/kg ip) hepatotoxicity progressing to centrilobular necrosis was studied by light and electron microscopy in Swiss white mice. Centrilobular glycogen depletion and cytoplasmic foaminess, usually accompanied by extensive vacuolation, were detectable by light microscopy 1 1/2 hr after furosemide. Centrilobular congestion and hydropic single cell necrosis developed after 3 hr. Electron microscopy revealed disaggregation of polyribosomes, vesiculation of endoplasmic reticulum, an endocytic origin for the vacuolation, and a definite sequence in the development of congestion. Vacuolation coincided with loss of microvilli and resulted in detachment of sinusoidal lining cells from hepatocytes. Small vacuoles apparently formed at the sinusoidal margin of hepatocytes by fusion of microvilli. Congestion and occlusion of sinusoidal lumens developed as a consequence of erythrocytes entering the enlarged Disse space, possibly through pores in the lining cells, and thence entering endocytic vacuoles. The vacuolation, loss of microvilli and terminal hydropic degeneration suggest an important role for the plasma membrane in the development of furosemide-induced hepatotoxicity. Comparisons with known membrane toxins support this concept.

Animals↗
PubMed1999

Effect of furosemide or mannitol before injection of a non-ionic contrast medium on intrarenal oxygen tension.

Oxygen tension (pO2) in rat renal cortex and outer medulla was studied after an intravenous injection of mannitol or furosemide, followed 10 minutes later by an intravenous injection of the non-ionic X-ray contrast medium (CM) iopromide (370 mg iodine/ml). Ten minutes after mannitol injection, before injection of CM, pO2 in the medulla had decreased from a control level of 32 +/- 3 to 28 +/- 4 mm Hg. The addition of CM caused a further decrease, to 24 +/- 5 mm Hg, which was a significant reduction. Ten minutes after furosemide injection the pO2 in the medulla had increased significantly, from a control value of 32 +/- 2 to 44 +/- 4 mm Hg. Injection of CM caused a significant decrease in pO2 to 37 +/- 3 mm. Ringer's solution (n = 6) caused no changes. We conclude that pretreatment with mannitol or furosemide does not prevent the CM-induced decrease in pO2 in the outer medulla.

Animals↗
PubMed1986

Effect of furosemide on the rat submandibular gland kallikrein secretion.

The effects of furosemide and Captopril were studied in normals and nephrectomized rats. Different doses of furosemide (5 to 50 mg/kg) increased the saliva kallikrein activity of submaxillary gland perfused with pilocarpine. Rats injected with captopril (10 mg) increased the blood flow of the gland, but did not modify the blood pressure. After furosemide (50 mg/kg) and captopril (10 mg), a decrease in arterial blood pressure was observed. The results suggest a release of glandular kallikrein which is secreted from the gland directly into the vascular compartment. On the other hand, rats sialodectomized showed no alterations in blood pressure in response to both drugs. These data suggest that submaxillary gland kallikrein play a role in regulating blood flow of the gland and blood pressure, at least in our experimental conditions.

Animals↗
PubMed1995

Furosemide disposition in patients on CAPD.

Single doses of oral and intravenous furosemide were given to 8 healthy male volunteers (40 mg) and 11 patients with renal failure maintained on continuous ambulatory peritoneal dialysis (CAPD) (80 mg). In the volunteers, absorption was variable. Only one half of the intravenous dose and one third of the oral dose was available for renal pharmacological action as judged by the urinary recovery. In the patients, absorption was also variable and was markedly delayed (tmax 128 vs 90 min) but more complete (bioavailability 70.1 vs 53.6%). The differences between the two groups were not significant, however (95% C.I.: -90 to 30 and -40.4 to 7.5 respectively). The mean elimination half-life was significantly longer in the patients following both the oral (228 vs 65.1 min) and intravenous dose (195 vs 60.3 min). The total body clearance of furosemide in the volunteers was 138 ml x min(-1) and this was much lower in the CAPD patients (61.9 ml x min(-1)) in whom the renal clearance was negligible. Although there were trends indicating differences in absorption between the two groups, the significant differences in furosemide disposition observed in CAPD patients were due to renal failure.

Absorption↗
PubMed1993

Torasemide versus furosemide in cirrhosis: a long-term, double-blind, randomized clinical study.

The effects of long-term therapy (70 days) with torasemide (20 mg/day), a new loop diuretic, were compared with those of furosemide (50 mg/day) in a randomized double-blind trial. Both drugs were administered in association with spironolactone (200 mg/day) in 28 nonazotemic cirrhotic patients with controlled ascites. The treatments did not modify creatinine clearance and exhibited a similar effect on body weight, urinary volume, and fractional excretion of uric acid, sodium, and chloride. The effect of torasemide on fractional potassium excretion was lower than that of furosemide. Torasemide showed higher sparing effect than furosemide on calcium, inorganic phosphate, and magnesium excretion and stronger action on free water clearance. No changes in serum parameters were induced by either treatment. Two episodes of hepatic encephalopathy occurred in the torasemide group. In view of its effects on sodium and water excretion and on other urinary parameters, torasemide can represent an alternative tool for the long-term treatment of ascites.

Ascites↗
PubMed1990

A comparison of the reduction in the K+ activity of the scala media produced by furosemide and ouabain.

The endocochlear potential (EP) and the K+ activity in the scala media of the guinea pig were recorded by means of K(+)-sensitive, double-barrelled microelectrodes in the second turn of the cochlea. EP and K+ change were recorded during the perilymphatic perfusion of furosemide and ouabain. Furosemide produced less of a decrease than ouabain in the K+ activity relative to the EP decrease. These results suggest that furosemide reduces the EP via different mechanisms from the inhibition of the K+ secretion potential.

Action Potentials↗