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Kinetics and dynamics of furosemide and slow-acting furosemide.

Bioavailability and dynamics of a sustained-release preparation of furosemide (FR, 60 mg) were compared with those of a conventional tablet (F, 40 mg). The preparations were given to 12 healthy subjects in a study of crossover randomized design once daily for a week. FR absorption was substantially delayed and the uptake of furosemide was about 75% of that from F, despite the larger dose administered. F induced a brief, intense diuresis and excretion of Na+, K+, and Cl-, both during short- and long-term administration. There was no such peak after FR. Total diuretic and saluretic effects did not differ between the two preparations, despite the lower bioavailability of FR. It is suggested that this discrepancy might be caused by transient supramaximal urinary levels of furosemide after F, whereby not all of the drug can exert an effect.

Adult↗

Comparison of the efficacy of furosemide with two furosemide-triamterene combinations in the treatment of cardiac insufficiency.

Nine patients suffering from cardiac insufficiency were given furosemide and two furosemide-triamterene combination products in random order. A statistically significant diuretic response was achieved with all these preparations. The combination of furosemide and triamterene brought about a 'softer' diuresis, no hypokalaemia and the advantage of dosage as only one tablet, thus eliminating the need for taking two separate drugs.

Aged↗

Determination of bioequivalence of two furosemide preparations; the effect of high doses of furosemide on some pharmacokinetic parameters.

The bioequivalence of two oral preparations of the diuretic furosemide, namely (i) a Croatian pharmaceutical product (test preparation A) and (ii) a reference preparation B, both in a dose of 500 mg was assessed in an open, cross-over, randomized trial in 15 healthy male volunteers, in whom the HPLC method with a fluorescent detector was used to determine its concentrations. The test preparation (A) was found to achieve a considerably higher concentration (17.2 +/- 9.304 mg/l) than the reference preparation (11.1 +/- 6.484 mg/l); the time to peak concentrations was statistically significantly shorter for the test preparation (1.033 +/- 0.743 h) than for the reference preparation (1.656 +/- 0.586), and the areas under the concentration curves were statistically significantly greater for the examined preparation (65.9 mg.h/l) than for the reference preparation (46.845 mg.h/l). The relative bioavailability of the test preparation was 129%, i.e. it was not bioequivalent with the reference preparation. This finding was consistent with the previously performed laboratory quality testing in vitro, where the release of the reference preparation was found to be considerably slower and weaker than that of the test preparation. High doses of furosemide exemplified by 500 mg were found to affect only some of the pharmacokinetic parameters, i.e. they induce an accelerated absorption, an increase in serum concentration, and a prolongation of its half-life.

Adult↗

Brain natriuretic peptide enhances renal actions of furosemide and suppresses furosemide-induced aldosterone activation in experimental heart failure.

BACKGROUND: The renal actions of brain natriuretic peptide (BNP) in congestive heart failure (CHF) are associated with increased diuresis and natriuresis, preserved glomerular filtration rate (GFR), and lack of activation of the renin-angiotensin-aldosterone system (RAAS). In contrast, diuretic-induced natriuresis may be associated with reduced GFR and RAAS activation. The objective of this study was to test the hypothesis that exogenous BNP enhances the renal diuretic and natriuretic actions of furosemide (Fs) and retards the activation of aldosterone in a model of CHF. METHODS AND RESULTS: CHF was produced in 2 groups of dogs by ventricular pacing. One group received continuous (90-minute) intravenous Fs (1 mg x kg(-1) x h(-1)). A second group (Fs+BNP) received 45-minute intravenous coinfusion of Fs (1 mg x kg(-1) x h(-1)) and low-dose (2 pmol x kg(-1) x min(-1)) BNP followed by 45-minute coinfusion of Fs (1 mg x kg(-1) x h(-1)) and high-dose (10 pmol x kg(-1) x min(-1)) BNP. Fs increased urinary flow, but the effect of Fs+BNP was greater. Similarly, urinary sodium excretion was higher in the Fs+BNP group. Although GFR tended to decrease in the Fs group, it increased in the Fs+BNP group (35+/-3 to 56+/-4*) (* indicates P<0.05 versus baseline) (P<0.0001 between groups). Plasma aldosterone increased with Fs (41+/-10 to 100+/-11* ng/dL) but was attenuated in the Fs+BNP group (44+/-11 to 54+/-9 ng/dL low-dose and to 47+/-7 ng/dL high-dose) (P=0.0007 between groups). CONCLUSIONS: Fs+BNP has more profound diuretic and natriuretic responses than Fs alone and also increases GFR without activation of aldosterone. Coadministration of BNP and loop diuretic is effective in maximizing natriuresis and diuresis while preserving renal function and inhibiting activation of aldosterone.

Animals↗

[Comparative study of pharmacokinetics and effects on urinary secretion of electrolytes of furosemide and furosemide-amiloride in healthy subjects].

A randomized cross over study was carried out in 12 healthy volunteers to investigate simultaneously the pharmacokinetics and the effects on urinary volume and electrolyte excretion after administration of single doses of 40 mg frusemide and a combination tablet containing both 40 mg frusemide and 5 mg amiloride. From a statistical analysis of plasma levels of frusemide and amiloride measured by HPLC methodology, no significant difference between the reference drug alone, frusemide, and the combination tablets was observed in mean peak plasma levels, mean times to peak or mean areas under the plasma concentration-time curves (AUC). Frusemide and the combination tablet both produced a rapid and powerful diuresis in the 0-2 hours postdose period and did not differ significantly in urine output at any time point. However a difference in natriuretic activity was observed between frusemide and the combination with the latter producing a significantly greater sodium excretion in the 0 to 2 hours period (p less than 0.05). Potassium retaining activity throughout the 24 hours was marked after the administration of the combination, the potassium excretion being significantly less (p less than 0.05) than either control of frusemide alone. There was also a significant correlation between plasma levels of frusemide and the time course of urine and electrolyte excretion in healthy subjects.

Adult↗

High-performance liquid chromatographic determination and identification of acyl migration and photodegradation products of furosemide 1-O-acyl glucuronide.

Stability of furosemide glucuronide, the major metabolite of furosemide, was studied in order to accurately assess the glucuronidation of furosemide. Furosemide glucuronide was purified by high-performance liquid chromatography, and the mass spectrum of furosemide glucuronide showed the molecular ion peaks [M-H]- at 505 and 507 (m/z). Furosemide glucuronide was photodegraded to the compound, which was shown more hydrophilic than furosemide glucuronide by high-performance liquid chromatography assay. The photodegradation product of furosemide glucuronide was hydrolyzed to one of the photodegradation products of furosemide by beta-glucuronidase, indicating that the photodegradation product of furosemide glucuronide possessed a glucuronic acid moiety. Furthermore, the mass spectrum of the photodegradation product of furosemide glucuronide exhibited molecular ion peaks [M-H]- at 487 and [M-2H+2Na]- at 509, indicating the chlorine displacement of furosemide glucuronide by a hydroxyl group. Furosemide glucuronide was unstable in an aqueous solution (pH=7.4), and presumed acyl migration isomers of furosemide glucuronide (furosemide glucuronide-isomers) were detected by high-performance liquid chromatography equipped with photodiode array UV detector. The UV spectra of seven furosemide glucuronide-isomers were closely similar to that of furosemide glucuronide but not furosemide. Exposing a mixture of furosemide glucuronide and furosemide glucuronide-isomers to light resulted in the production of new compounds. UV spectra of photodegradation products of furosemide glucuronide-isomers were closely similar to those of photodegradation product of furosemide glucuronide. These results suggested that furosemide glucuronide-isomers were also photodegraded, resulting in the displacement of chlorine by a hydroxyl group as in furosemide glucuronide.

Chromatography, High Pressure Liquid↗

Toxicology and Carcinogenesis Studies of Furosemide (CAS No. 54-31-9) in F344/N Rats and B6C3F1 Mice (Feed Studies).

Furosemide is a diuretic used in human and veterinary medicine. Toxicology and carcinogenesis studies were conducted by feeding diets containing furosemide (99% pure, USP grade) to groups of F344/N rats and B6C3F1 mice of each sex for 14 days, 13 weeks, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, mouse L5178Y lymphoma cells, and Chinese hamster ovary (CHO) cells. Fourteen-Day and Thirteen-Week Studies: Dietary concentrations of furosemide used in the 14-day studies for rats and mice ranged up to 46,000 ppm. Two of five male and 3/5 female rats that received 46,000 ppm furosemide died before the end of the studies. Rats that received 15,300 or 46,000 ppm lost weight over the course of the studies. The final mean body weights of rats that received 1,700 or 5,100 ppm were 12% or 23% lower than that of controls for males and 8% or 16% lower for females. Nephrosis was dose related in rats. All five male and 1/5 female mice that received 46,000 ppm furosemide died before the end of the 14-day studies. Male mice that received 15,300 ppm and female mice that received 46,000 ppm lost weight. The final mean body weights of male mice that received 1,700 or 5,100 ppm were 16% or 14% lower than that of controls. The final mean body weight of females that received 15,300 ppm was 13% lower than that of controls. Slight dilatation of the renal cortical tubules and/or nephrosis were dose related in mice. Dietary concentrations of furosemide used in the 13-week studies were 0 and 625-10,000 ppm for male rats and 0 and 938-15,000 ppm for female rats and male mice. Concentrations for female mice were 0 and 1,250-20,000 ppm. None of the rats died before the end of the studies. The final mean body weights of male rats that received 2,500, 5,000, or 10,000 ppm furosemide were 11%, 22%, or 44% lower than that of controls. The final mean body weights of female rats that received 3,750, 7,500, or 15,000 ppm were 18%, 26%, or 35% lower than that of controls. Minimal-to-mild nephrosis occurred in the two highest dose groups of male and female rats. Mineralization of minimal to mild severity was observed at the renal corticomedullary junction in dosed male rats receiving 625 ppm or more; the severity and incidence of the mineralization increased with increased dose. No compound-related deaths occurred in mice. The final mean body weights of male mice that received 3,750, 7,500, or 15,000 were 12%, 22%, or 17% lower than that of controls. Final mean body weights of dosed and control female mice were comparable. Compound-related lesions in mice induced minimal-to-mild nephrosis. Because of the lower body weights and the kidney lesions in the 13-week studies, doses selected for the 2-year studies were 0, 350, or 700 ppm furosemide in the diet for groups of 50 F344/N rats of each sex. Groups of 50 B6C3F1 mice of each sex were fed diets containing 0, 700, or 1,400 ppm furosemide for 104 weeks. Body Weight and Survival in the Two-Year Studies: Mean body weights of dosed and control rats were comparable throughout the studies. No significant differences in survival were observed between any groups of rats of either sex (final survival--male: control, 17/50; low dose, 17/50; high dose, 20/50; female: 35/50; 31/50; 34/50). The final survival of all groups of male rats was low, reflecting the large number of moribund animals killed after week 91. Survival at week 90 was 35/50, 28/50, and 34/50. Mean body weights of high dose male mice were up to 17% lower than those of controls, and mean body weights of low dose male mice were about 5%-10% lower than those of controls after week 31. Mean body weights of high dose female mice were up to 22% lower than those of controls. Mean body weights of low dose female mice were 5%-13% lower than those of controls after week 82. The survival of the high dose group of female mice was significantly lower than that of controls after week 99 (final survival--male: 31/50; 24/50; 26/50; female: 36/50; 29/50; 18/50). Feed consumption by dosed rats was similar to that by controls. The estimateer week 99 (final survival--male: 31/50; 24/50; 26/50; female: 36/50; 29/50; 18/50). Feed consumption by dosed rats was similar to that by controls. The estimated average amount of furosemide consumed per day was approximately 14-16 or 29-31 mg/kg for low dose or high dose rats. Feed consumption by dosed mice was approximately 5&percnt;-7&percnt; greater than that by controls. The average amount of furosemide consumed per day was approximately 91-99 or 191-214 mg/kg for low dose or high dose mice. Nonneoplastic and Neoplastic Effects in the Two-Year Studies: Nephropathy occurred at similar incidences in all groups of rats, but the severity was greater in dosed male rats. Tubular cell hyperplasia was observed in 4/50 control, 2/50 low dose, and 4/50 high dose male rats. Tubular cell adenomas of the kidney occurred in 1/50 control, 3/50 low dose, and 1/50 high dose male rats. Tubular cell adenocarcinomas were seen in a fourth low dose male rat and in a second high dose male rat (adenomas or adenocarcinomas, combined: control, 1/50; low dose, 4/50; high dose, 2/50). The historical incidence of renal tubular cell adenomas or adenocarcinomas (combined) in untreated male F344/N rats is 9/1,928 (0.5&percnt;), and the highest incidence observed in controls is 3/50. Malignant meningiomas of the brain occurred in 3/50 low dose male rats; none was observed in other groups. The historical incidence of meningiomas in untreated male F344/N rats is 2/1,928 (0.1&percnt;). C-Cell adenomas of the thyroid gland in female rats occurred with a positive trend; the incidence in the high dose group was not statistically greater than that in the controls (4/50; 6/50; 11/50). A C-cell carcinoma occurred in another low dose female rat. The incidence of adenomas of the anterior pituitary gland in low dose male rats was marginally greater than that in controls (4/50; 11/50; 8/50). Neither of these marginal increases was considered to be chemically related. Malignant mixed tumors (adenocarcinoma, type C) of the mammary gland occurred in dosed female mice (0/50; 1/50; 5/48). One mammary gland acinar cell carcinoma occurred in a second low dose female mouse. The historical incidence of all malignant mammary gland neoplasms in untreated female B6C3F1 mice is 40/2,040 (2&percnt;). Compound-related nonneoplastic lesions of the kidney in mice included nephropathy and dilatation of the renal pelvis for males and females and tubular cysts, suppurative inflammation, and epithelial hyperplasia of the renal pelvis for males. Kidney lesions may have contributed to the low survival of high dose female mice. Mucosal epithelial hyperplasia and submucosal chronic focal inflammation of the urinary bladder were observed at increased incidences in dosed male mice. Suppurative inflammation of the prostate was observed at an increased incidence in high dose male mice. Fighting may have contributed to urogenital lesions in male mice. Suppurative inflammation of the ovary or uterus was observed at an increased incidence in high dose female mice. Hematopoiesis was observed at increased incidences in the spleen and liver of dosed male and high dose female mice and in the adrenal cortex of high dose female mice. Genetic Toxicology: Furosemide was not mutagenic in S. typhimurium strains TA98, TA100, TA1535, or TA1537 when tested with or without exogenous metabolic activation. In the mouse lymphoma assay for trifluorothymidine (Tft) resistance, furosemide produced an equivocal response in the absence of metabolic activation and a positive response in the presence of activation. Furosemide induced sister chromatid exchanges and chromosomal aberrations in CHO cells in both the presence and absence of exogenous metabolic activation. Audit: The data, documents, and pathology materials from the 2-year studies of furosemide have been audited. The audit findings show that the conduct of the studies is documented adequately and support the data and results given in this Technical Report. Conclusion: Under the conditions of these 2-year feed studies, there was equivocal evidence of carcinogenic activity of furosemide for male F344/N rats, as shown by marginal increases in uncommon tubular cell neoplasms of the kidney and meningiomas of the brain. There was no evidence of carcinogenic activity of furosemide for female F344/N rats fed diets containing 350 or 700 ppm furosemide for 2 years. There was no evidence of carcinogenic activity for male B6C3F1 mice fed diets containing 700 or 1,400 ppm furosemide for 2 years. There was some evidence of carcinogenic activity of furosemide for female mice, as shown by an increase in malignant tumors of the mammary gland. Nephropathy was more severe in the kidney of male rats and of male and female mice fed diets containing furosemide than in controls. Synonyms: 5-(aminosulfonyl)-4-chloro-2-[(2-furanylmethyl)amino]benzoic acid; frusemide; fursemide Trade Names: Aisemide; Aluzine; Beronald; Desdemin; Diural; Dryptal; Errolon; Frusemin; Fulsix; Fuluvamide; Furosemide "Mita"; Katlex; Lasilix; Lasix; Lowpstron; Rosemide; Transit; Urosemide

Journal Article↗

Furosemide interactions with brain GABAA receptors.

1. The loop diuretic furosemide is known to antagonize the function of gamma-aminobutyric acid type A (GABAA) receptors. The purpose of the present study was to examine the direct interaction of furosemide with the GABAA receptors by autoradiography and ligand binding studies with native rat and human receptors and with recombinant receptors composed of rat subunits. 2. Autoradiography with [35S]-t-butylbicyclophosphorothionate ([35S]-TBPS) as a ligand indicated that furosemide (0.1-1 mM) reversed the 5 microM GABA-induced inhibition of binding only in the cerebellar granule cell layer of rat brain sections. In all other regions studied, notably also in the hippocampal and thalamic areas, furosemide failed to antagonize GABA. Furosemide 1 mM decreased [35S]-TBPS binding only in a limited number of brain regions, but facilitation of the GABA-inhibition of the binding was much more widespread. 3. In well-washed rat cerebellar, but not cerebrocortical, membranes, furosemide enhanced the [35S]-TBPS binding over basal level in the absence of added GABA. The GABAA antagonist, SR 95531, and the convulsant, Ro 5-4864, blocked this furosemide-induced increase. Both interactions with the furosemide enhancement are likely to be allosteric, since furosemide affected the binding of [3H]-SR 95531 and [3H]-Ro 5-4864 identically in the cerebellar and cerebrocortical membranes. Maximal GABA-antagonism induced by furosemide in cerebellar membranes was further increased by SR 95531 but not by Ro 5-4864, indicating additive antagonism only for SR 95531. In human cerebellar receptors, only GABA antagonism by furosemide, but not the enhancement without added GABA, was observed. 4. In recombinant GABAA receptors, furosemide antagonism of GABA-inhibition of [35S]-TBPS binding depended only on the presence of alpha 6 and beta 2/3 subunits, irrespective of the presence or absence of gamma 2 or delta subunits. 5. In alpha 6 beta 3 gamma 2 receptors, clozapine reversed the enhancement of [35S]-TBPS binding by furosemide in the absence of GABA. However, it failed to affect the GABA-antagonism of furosemide, suggesting that the enhancement of basal binding and the GABA antagonism might represent two different allosteric actions of furosemide. 6. In conclusion, the present results indicate that furosemide is a subtype-selective GABAA antagonist with a mode of action not shared by several other antagonists, which makes furosemide a unique compound for development of potential GABAA receptor subtype-specific and -selective ligands.

Animals↗

Influence of meloxicam on furosemide pharmacokinetics and pharmacodynamics in healthy volunteers.

Fifteen healthy male volunteers participated in an open, multiple-dose study to investigate a possible interaction between furosemide and meloxicam, a new non-steroidal anti-inflammatory agent (NSAID). The study comprised three treatment periods. First, furosemide (40 mg) was administered as a single oral daily dose for 3 days. A wash-out day was followed by the administration of meloxicam (15 mg) as a single oral daily dose for 10 days. Thereafter, meloxicam and furosemide were administered concomitantly at the same doses as described above, for 3 days. The effect of concomitant ingestion of meloxicam and furosemide on furosemide-induced diuresis, urine and serum electrolytes, and furosemide pharmacokinetics was determined, after both single and repeated administration of furosemide. Estimates of the "(furosemide+meloxicam)/(furosemide alone)" mean ratio of the variable AUC(0-infinity) for plasma furosemide and the cumulative sodium excretion (0-8 h) were 97.4% (90% confidence interval 89.7-106%) and 88% (90% confidence interval 82-94%), respectively. The study results indicate that meloxicam does not affect the pharmacokinetics of furosemide in healthy volunteers, nor does it affect furosemide-induced diuresis or serum electrolytes. The cumulative urinary electrolyte excretion after concomitant administration of meloxicam and furosemide is somewhat lower than after administration of furosemide alone, in particular for the period 0-8 h after administration of furosemide. This effect of meloxicam on furosemide dynamics is small, and is probably not clinically relevant in healthy volunteers under the dosing regime studied.

Administration, Oral↗