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 19 recordsLinked to original sources

PubMed1979

Effect of furosemide (lasix) on acute severe experimental cerebral edema.

The effect of furosemide (Lasix) therapy on a standardized experimental cerebral edema, induced in rats by applying a cooling stamp to the right side of the skull over the right coronal suture by means of a stereotactic instrument, was examined. The hemispherically separated water and electrolyte contents of the brain were analyzed after 24 h. Following furosemide therapy, the behavior of these edema parameters was compared statistically with dexamethasone, glycerol and albumin. An increase of the water and sodium content, and a decrease of potassium was observed 24 h after the trauma, especially in the right hemisphere. Furosemide did not improve either the water content or the electrolyte balance. By contrast, the administration of dexamethasone, glycerol and albumin was followed by a significant improvement of the edema. In experiments with cats, the course of the edema and the effect of furosemide on the cold brain injury of the right hemisphere were observed by measuring the intracranial pressure (ICP) values, and by continuous monitoring of the EEG. The ventricular CSF pressure and epidural pressures were also recorded. The electrical brain activity was continuously compared with the course of the ICP by means of computer analysis. In addition, the blood osmolality and diuresis were monitored. The ICP increased rapidly after the trauma, establishing considerable pressure gradients, and the EEG power intensities decreased markedly on the right side. Histologically, there was an extended edema of the white matter of both hemispheres. The ICP was not lowered by single injections or high dose infusions of furosemide, and the EEG power intensities also did not improve. Infusions of large volumes of furosemide even resulted in an increase of ICP, but infusion of 40% sorbitol effected a rapid decrease of ICP and EEG recovery over the left hemisphere. Sorbitol infusion also caused a marked rise in the blood osmolality, whereas furosemide had no such effect. The results raise considerable doubts as to the propriety of the exclusive use of furosemide for cases of acute cerebral edema with raised ICP. The diuretic effect is insufficient to establish an osmotic gradient, and its general dehydrating effect does not acutely influence the ICP. The absence of effect on the experimental tissue edema would not appear to commend furosemide as basic therapy for cases of traumatic cerebral edema.

Albumins↗

PubMed1979

Plasma and tissue levels of furosemide in dogs and monkeys following single and multiple oral doses.

35S-Furosemide was administered to beagle dogs and rhesus monkeys as an oral solution on a single and a 20 repeated 5 mg/kg/day dosing regimen. In both species, furosemide is rapidly but incompletely absorbed with peak plasma levels being achieved within one hour after dosing. The plasma level versus time profiles do not appear to be significantly altered as a result of the repetitive dosing regimen employed, although the profiles themselves are quite different for the two species studied. Following single oral doses, the observed peak plasma levels achieved in dogs are approximately eight-fold higher than in monkeys. In dogs, oral administration of furosemide results in a biexponential disposition curve while in monkeys the profile appears monoexponential. The major disposition phase in dogs has a half-life or approximately 30 minutes and is followed by a slow elimination phase with a half-life of approximately 7 hours. Only a small percentage of the absorbed dose is affected by the slow disposition phase and consequently accumulation of furosemide on the once-daily dosing regimen is slight. In the monkey studies, the rapid disposition phase was not observed and the slow disposition phase had a half-life of approximately 11 hours. On the repetitive dosing regimen, the monkey appeared to accumulate furosemide to a slightly greater extnet than the dog and showed a lesser degree of fluctuation within a dosing interval. In both species, liver and kidney radioactivity levels were not detectable three days after a single dose although low levels of furosemide and/or metabolites were observed for six days following the last dose of the multiple dosing regimen. At the dosage level and regimen employed, no unusual or "typical" lesions associated with furosemide were found in the dog and monkey tissues examined histopathologically.

Administration, Oral↗

PubMed1976

[Cyclic AMP and plasma renin activity in renal vein blood after amitryptiline, theophylline, furosemide and beta adrenergic blocking substances (author's transl)].

The influence of amitryptiline, theophylline and furosemide on the concentration of cyclic-AMP and plasma renin activity (PRA) was investigated in renal vein plasma. Additionally, the stimulating effect of furosemide on the PRA after application of the beta-adrenergic receptor antagonists propranolol and practolol and the cyclic AMP concentration in the plasma were measured. All drugs were given intravenously. After amitryptiline cyclic-AMP concentration increased about 1.5-fold compared with the basal value,PRA was not altered. After theophylline cyclic-AMP concentration increased about 1.2-fold, PRA 2.0-fold compared with the basal value, PRA was not altered. After theophylline cyclic-AMP concentration increased about 1.2-fold, PRA 2.0-fold coa increased within 7 min and no further increase was observed till the 15th min. After practolol cyclic-AMP concentration and PRA decreased about 20% compared with the basal value within 10 min. The stimulating effect of subsequently applied furosemide on PRA was not altered, but the cyclic-AMP concentration was not changed in this time by furosemide. After propranolol cyclic-AMP concentration and PRA decreased about 20% compared with the basal value. The cyclic-AMP concentration was not influenced by the following furosemide application, in agreement with the findings after practolol, however, PRA could be stimulated only in 36% of these patients under beta-receptor blockade. Our results show that changes of the concentrations of cyclic-AMP and of PRA are independent of each other. An elevated intracellular cyclic-AMP level due to the inhibition of phosphodiesterase is as a single factor unable to stimulate renin release. Our results give no evidence of a direct involvement of the adenylcyclase-system in the mechanism of renin release. The effect of propranolol and practolol on the basal value of PRA and cyclic-AMP is equal. The different influence of 10 mg propranolol and 20 mg practolol on the stimulating effect of 40 mg furosemide on the PRA can be interpreted as a dosage problem.

Adrenergic beta-Antagonists↗

PubMed1977

Effects of ethacrynic acid and furosemide on phosphorylation reactions of kidney mitochondria. Inhibition of the adenine nucleotide translocase.

Previous reports that ethacrynic acid and furosemide diminish mitochondrial P : O ratios and reduce (Na+ + K+)-ATPase activity suggested that these diuretics may inhibit mitochondrial phosphorylation reactions. This possibility was initially studied by determining the effects of ethacrynic acid and furosemide on [32P]ATP exchange activity of rat kidney mitochondria. Concentrations of both drugs at 10(-4) M or greater, significantly inhibited [32P]ATP exchange. To investigate the mechanism of this inhibition, the effects of ethacrynic acid and furosemide on the ATPase activity of intract mitochondria and sonicated submitochondrial particles were determined. Both diuretics inhibited ATPase activity of intact mitochondria at 10(-4) M. In contrast, ATPase of submitochondrial particles was significantly less susceptible to inhibition by the diuretics. These results suggested that ethacrynic acid anf furosemide inhibit adenine nucleotide transport across the mitochondrial membrane. This was directly tested by determining the effects of the diretics on the mitochondrial adenine nucleotide translocase. At 5-10(-4) M, both ethacrynic acid and furosemide significantly inhibited adenine nucleotide transport. These findings suggest that ethacrynic acid and furosemide may diminish renal tubular solute reabsorption by direct inhibition of adenine nucleotide transport across the mitochondrial inner membrane.

Adenosine Triphosphatases↗

PubMed2026

Efficacy and safety of human albumin combined with furosemide in acute decompensated heart failure with hepatic dysfunction.

BACKGROUND: Congestion is the most common clinical presentation on admission of patients with acute decompensated heart failure (ADHF). Finding effective ways to alleviate congestion has become a pivotal management step. This study sought to investigate the efficacy and safety of intravenous (IV) albumin use in conjunction with furosemide in patients hospitalized for ADHF with hepatic dysfunction in terms of subjective regression of congestion symptoms and worsening renal function. METHODS: This prospective, open-label, randomized-pragmatic trial recruited 241 patients with hepatic dysfunction hospitalized for ADHF. Patients (78 years, 54% female) were assigned to receive IV albumin with furosemide or IV furosemide alone. The coprimary study endpoints were patients' global assessment of symptoms score, quantified as the area under the curve (AUC) of the score on a visual analog scale, and the change in creatinine levels over 72 hours from admission. RESULTS: The experimental treatment group demonstrated a greater improvement in patients' global assessment of symptoms scores (AUCbaseline-72 h 3,767 vs 3,457 points; P < .001) and a milder increase in creatinine levels (0.07 vs 0.18 mg/dL; P = .045) than the IV furosemide group. The length of stay was 1 day shorter (4 vs 5 days; P < .001) and the incidence of worsening renal function was lower (25% vs 38%; P = .037) in the experimental treatment group. CONCLUSIONS: In this hypothesis generating study, among patients with ADHF and hepatic dysfunction, concomitant use of IV albumin and furosemide for the first 72 hours resulted in a significant improvement in subjective perception symptoms of decongestion and a milder increase in creatinine levels than IV furosemide alone.

Aged↗

PubMedDate not supplied

Biotransformation of furosemide in patients with acute pulmonary edema.

Furosemide (20-80 mg) was administered iv over 5 min to 16 patients with the diagnosis of acute pulmonary edema due to left heart failure. Serum and urine samples collected during the 24 hr after administration were assayed for furosemide and its biotransformation products by gas-liquid chromatography. A biexponential decay of serum furosemide concentrations vs. time was observed. Recovery of furosemide and its metabolites from urine in 24 hr varied between 30 and 98% of the administered dose. The excretion of unchanged drug accounted for 22.6-73.4% of the dose. The excretion of the glucuronide metabolite and 2-amino-4-chloro-5-sulfamoylanthranilic acid accounted for 3.3-40.4% and from 0.13-3.92% of the dose, respectively. Urinary excretion of furosemide was less in patients with, than in those without, myocardial infarction. Urinary excretion of the oxidative acidic metabolite was increased in patients with reduced creatinine clearance. The glucuronide metabolite of furosemide was the major biotransformation product in these patients with acute pulmonary edema.

Acute Disease↗

PubMed1978

The pharmacologic effects of furosemide therapy in the low-birth-weight infant.

The pharmacologic effects of furosemide were studied in six infants (mean gestation 30.7 weeks; mean birth weight 1,490 gm) at ages 10 to 57 days. Furosemide (for clinical indication, standardized at 1 mg/kg) was given intravenously over one minute; data were collected over the ensuing 24 hours. For three hours following furosemide administration, a significant diuresis was observed. Sodium excretion, percent fractional sodium excretion, and potassium excretion were significantly increased and urinary pH significantly decreased for six hours following the administration of furosemide. Creatinine and free water clearances were slightly elevated, although not significantly. Furosemide is an effective diuretic, the onset of pharmacologic action was within one hour, the peak action was sustained for three hours, and the duration of action was six hours. The net fluid, sodium, and potassium losses following a 1 mg/kg single dose were 28 ml, and 3.6 and 0.3 mEq/kg, respectively.

Furosemide↗

PubMed1976

Biochemical changes after hepatic injury from toxic doses of acetaminophen or furosemide.

The effects of hepatotoxic doses of acetaminophen and furosemide on the function and composition of hepatic endoplasmic reticulum were compared from 3 to 24 h after administration. Acetaminophen caused a significant decrease in microsomal protein concentration as early as 3 h after its administration, but furosemide did not affect the microsomal protein concentration until 24 h after the dose. Both acetaminophen and furosemide decreased the concentrations of cytochrome P-450 and cytochrome b5 in microsomes, and the activity of microsomal ethylmorphine N-demethylase and aniline hydroxylase. Glucose-6-phosphatase and UDP-glucuronyl transferase were not significantly affected by acetaminophen or furosemide administration, and neither diene conjugation nor hepatic triglycerides were increased. Incorporation of 3H-L-leucine into liver proteins was decreased by 50% after the administration of either acetaminophen or furosemide.

Acetaminophen↗

PubMed1977

The effect of furosemide on the flow and composition of bile in the dog.

The effect of furosemide, a potent inhibitor of active sodium transport, on the amount and composition of bile was studied in the dog. Ten milligrams per kilogram of body weight of furosemide were injected intravenously to anesthetized dogs with a previously constructed fistula of the common bile duct. In all dogs, a 2.5 times increase in bile flow was observed concomitant with a 15 times increase in urinary output. The amount of bile flow decreased gradually and returned to control levels 60 to 75 minutes after furosemide injection. The choleretic effect was associated with a high increase in sodium, chloride and bicarbonate anions and with a smaller increase in potassium, phosphorus and calcium. The total amount of bilirubin alkaline phosphatase and cholesterol was not significantly affected, while the calculated output of inorganic salts increased. The results indicate that inhibition of sodium reabsorption by furosemide simultaneously affects the liver and kidney and that the increase in electrolyte solution is most likely caused by the inhibition of sodium reabsorption in the ductuli. Furosemide also may interfere with the sodium mediated secretory fraction at the canalicular level, but the predominant factor determining the increase in bile flow and electrolytes is inhibition of sodium reabsorption in the biliary ducts and ductuli.

Alkaline Phosphatase↗

PubMed1975

Furosemide, mithramycin, and salmon calcitonin in hypercalcemia.

Twenty-nine patients with acute hypercalcemia secondary to carcinoma, myeloma and parathyroid adenoma have been treated with large doses of furosemide, mithramycin, or salmon calcitonin perfusion. With furosemide administration the treatment was successful in 6 of 10 patients. Furosemide was injected intravenously at the rate of 125 mg every 3 hours. With mithramycin perfusion only 2 of 8 patients have a return of the serum calcium levels to normal. With salmon thyrocalcitonin 3 of 10 patients obtained a good result. It can be interesting to suggest the association of furosemide and salmon calcitonin infusion to treat hypercalcemia of myeloma.

Adenoma↗

PubMed2026

Comparative effectiveness of torsemide vs furosemide in the management of heart failure patients: Win-ratio reanalysis of the TRANSFORM-HF trial.

BACKGROUND: Loop diuretics are widely used for managing congestion in patients with heart failure (HF). The TRANSFORM-HF trial is a multicenter randomized study that enrolled heart failure patients, comparing a strategy of torsemide vs furosemide. The time-to-event analysis demonstrated neutral effects on all-cause death at 30 months and the composite of all-cause death and first rehospitalization at 12 months. We evaluated whether a hierarchical win-ratio (WR) framework integrating mortality, recurrent hospitalization, and patient-reported health status provides additional interpretive insight. METHODS: This study is a secondary analysis of the pragmatic, multicenter, open-label, randomized TRANSFORM-HF trial, conducted across 60 US hospitals that randomized 2,859 patients hospitalized with HF to torsemide or furosemide. The primary 12-month hierarchical composite outcome was defined as (1) all-cause mortality, (2) recurrent all-cause hospitalizations, and (3) lack of improvement in the Kansas City Cardiomyopathy Questionnaire Clinical Summary Score (KCCQ-CSS). The primary statistical method was a WR analysis adjusting covariates via inverse probability weighting. Subgroup analyses evaluated potential heterogeneity across patient demographics and clinical characteristics. RESULTS: In the primary 12-month intention-to-treat analysis, the adjusted WR was 1.07 (95% CI, 0.98-1.16; P = .13), indicating no significant difference between torsemide and furosemide. A supplementary 30-month analysis with extended mortality follow-up yielded a similar estimate (adjusted WR, 1.06; 95% CI, 0.98-1.16; P = .14); hospitalization and KCCQ-CSS components were assessed through 12 months. As-treated sensitivity analyses were consistent with the neutral primary findings. Exploratory subgroup analyses were not adjusted for multiplicity and should be considered hypothesis-generating. CONCLUSIONS: The overall WR comparison between torsemide and furosemide showed no statistically significant difference in the primary 12-month analysis. The WR framework provided an interpretive decomposition across outcome domains but did not establish superiority of either loop diuretic strategy. All findings should be considered exploratory. TRIAL REGISTRATION: ClinicalTrials.gov, NCT03296813, https://clinicaltrials.gov/study/NCT03296813.

Aged↗

PubMed1978

A simplified assay of furosemide in plasma and urine by high-pressure liquid chromatography.

A simplified high-pressure liquid chromatograhic method for determination of furosemide in plasma and urine has been developed using a fluorometric detector directly coupled to the column effluent. The method includes an ether extraction from acidified biologic samples. The mobile phase used for chromatography on a reversed-phase column (C15 hydrocarbon permanently bonded to silica particles) is sufficiently acidic to induce fluorescence of furosemide. The methylester of furosemide is employed as an internal standard. The sensitivity is 0.1 and 0.25 microgram per ml plasma and urine, respectively. The applicability to pharmacokinetic studies of furosemide is shown.

Adult↗

PubMed1975

[Evoked response audiometry of the guinea pig before and after drop in hearing induced by furosemid (author's transl)].

Using particular surface electrodes evoked response audiometry (ERA) can be applied to small laboratory animals without any sedation or anaesthesia. In addition to other methods we have studied in this way the influence of extreme doses of Furosemid on the guinea pig inner ear. 6-20 mg Furosemid per 100 g of bodyweight (about 100 times the human therapy dose) were applicated i.v. within 5 min resulting in a drop of hearing immediately. For the anaesthesized animal the cochlear microphonic potentials (CM) decrease simultaneously, indicating Furosemid to act at the inner ear itself. By both methods recovery of inner ear function is seen to start about 10 min later according to the little biological half life of Furosemid. As being restricted in respect of time for the CM-measurements we are sure about reversibility only by the ERA-method.

Animals↗

PubMedDate not supplied

[Succinate dehydrogenase and Na+-K+-ATPase activities in cells of rat kidney tubules during increased excretion of sodium, caused by furosemide].

In the cells of nephron tubules an effect of furosemide on kidney function and on succinate dehydrogenase and Na+-K+-ATPase activities was studied cytochemically. Administration of furosemide (1 mg per 100 g of body weight) increased excretion of sodium and potassium. If the rate of filtration through Malpighian tufts was constant, the increase in Na and K excretion demonstrated the tubular effect of the diuretics. Both administration of furosemide and preincubation of the drug with kidney slices in vitro caused a decrease in succinate dehydrogenase activity in the cells of all the nephron sections. These data suggest that a direct effect of the diuretics on oxidative metabolism in renal cells took place. Alteration in the activity of Na+-K+-ATPase was observed only in vivo and in those nephron sections, where sodium reabsorption was decreased under the effect of furosemide.

Adenosine Triphosphatases↗

PubMed1975

[Age-dependent biochemical studies on the extrarenal effect of furosemid (author's transl)].

The present study investigated the activities of lysosomal enzymes of the liver after administration of Furosemid. 10 weeks and 1-year old male albino rats were treated with 40 mg Furosemid for 4 subsequent days. According to the method devised by de Duve a sediment rich in lysosomes was produced by fractionated centrifugation and subsequently the enzyme activity of beta-glucuronidase, beta-acetylglucosaminidase, cathepsin D and a collagenolytic enzyme was measured in the sediment as well as in the corresponding lysosomal supernatant. The protein content served as a reference for the enzyme activities. In addition, we investigated the activities of cytoplasmic enzymes such as GOT, GPT, gamma-GT and the alkaline phosphatase. The enzyme activity changes were age-dependent. With Furosemid treatment the activities of beta-glucuronidase and cathepsin D increased in the lysosomal supernatant and the lysosomal sediment of the 1-year old rats, whereas the activities of the collagenolytic enzyme increased in the lysosomal sediment of the same group. In the lysosomal sediment of the 10-weeks old rats a decrease of beta-glucuronidase, beta-acetylglucosaminidase and cathepsin D was observed. These results are discussed in the light of reports from the literature.

Age Factors↗

PubMed1977

Effect of chronic furosemide administration on hydrogen and sodium excretion in the dog.

Studies were performed to evaluate the effects of the chronic administration of furosemide on hydrogen and electrolyte excretion in dogs on a normal electrolyte diet and in the absence of electrolyte or volume depletion. Control daily excretion in five dogs averaged 64 meq for Na, 51 meq for K, 66 meq for Cl, and 17 meq for net H. Furosemide, 40 mg, in the drinking water 3 times daily was given for 4 days. On day 1 Na excretion averaged 128 meq, but thereafter was not significantly different from control levels. Over 4 days cumulative net H excretion increased 63.6 meq and plasma HCO3 rose 6.6 meq/liter. The same dogs were restudied by the same protocol except that, to obviate electrolyte depletion, NaCl and KCl were administered daily in quantities sufficient to replace urinary losses. All dogs remained in positive Na, K, and Cl balance. Body weight, hematocrit, plasma albumin, creatinine, and plasma renin activity were unchanged, indicating the absence of electrolyte or volume depletion. Nonetheless, cumulative net H excretion increased 61.2 meq and plasma HCO3 increased 4.3 meq/liter. Two adrenalectomized dogs receiving steroid replacement showed similar changes in net H excretion and plasma HCO3. These experiments suggest that chronic furosemide administration may enhance H excretion and generate alkalosis even in the absence of volume or electrolyte depletion and without increased aldosterone secretion.

Acid-Base Equilibrium↗

PubMed1975

[Effect of d-1 propranolol on urinary osmolarity after furosemide in anesthesized dog].

The effects of propranolol (l mg/kg/H infused in the renal artery) on the diuretic action of furosemide (20 mg/kg i.v.) have been studied in pentobarbital anesthetized dogs. We obtained the 3 following results : the urine remained isotonic to the plasma during the 6 hours following the furosemide injection ; the urinary output of sodium and water, measured during 6 hours after furosemide injection, was increased ; the renin hypersecretion was inhibited.

Animals↗

PubMed1976

An experimental and clinical pharmacological study of the influence of triamterene on the diuretic and saluretic properties of furosemide xantinol.

The diuretic and saluretic effect of furosemide xantinol administered alone and mixed with different amounts of 2,4,7-triamino-6-phenylpteridine (triamterene) have been investigated in rat and man. The presence of triamterene resulted in a dose dependent inhibition of furosemide xantinol induced diuresis in both species. It was necessary to reduce the amount of triamterene present in the mixture to approximately half that of the one theoretically required according to considerations of the recommended therapeutic doses of the two diuretics before significant inhibition was avoided. Nevertheless, this reduced amount of triamterene proved sufficient to inhibit the distal tubular exchange of Na+ for K+ and H+ and a mixture formulated to give the ratio of 40 mg furosemide xantinol (as base) plus 25 mg triamterene (Salidur) was shown to produce a smooth but efficient loss of water and Na+ in the absence of detectable kaliuresis or reduction in urinary pH, thereby reducing the usual risk of inducing hypokalaemic alkalosis.

Adult↗