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PubMed1987

Immediate hemodynamic response to furosemide in patients undergoing chronic hemodialysis.

To evaluate the effect of furosemide on cardiovascular hemodynamics in patients with end-stage renal failure, we studied ten patients undergoing hemodialysis three times a week. Arterial pressure, heart rate, and cardiac output (indocyanine green dye) were measured in triplicate; total peripheral resistance and central blood volume were calculated by standard formulas. Hemodynamics were determined at baseline and 5, 10, 15, and 30 minutes after intravenous (IV) bolus injection of furosemide 60 mg. Furosemide produced a decrease in central blood volume of -13% +/- 2.2% from pretreatment values (P less than .01) that was most pronounced five minutes after injection, together with a fall in cardiac output (from 6.76 +/- 0.59 to 6.17 +/- 0.52 L/min, P less than .10). Stroke volume decreased with a maximum fall occurring after 15 minutes (from 84 +/- 7 to 79 +/- 7 mL/min, P less than .05), and total peripheral resistance increased (from 15.8 +/- 2.1 to 17.8 +/- 2.3 units, P less than .05) after furosemide. Arterial pressure and heart rate did not change. The decrease in central blood volume reflects a shift of the total blood volume from the cardiopulmonary circulation to the periphery, suggesting dilation of the peripheral venous bed. Thus, even in patients undergoing hemodialysis, furosemide acutely decreases left ventricular preload by venous dilation and should therefore prove to be beneficial in acute volume overload.

Adult↗
PubMed1982

Specimen handling and high-performance liquid chromatographic determination of furosemide.

A simple high-performance liquid chromatographic method to measure furosemide in plasma and urine is described. Furosemide fluoresces best, but is unstable, at acidic pH and is subject to photochemical degradation. These factors were analysed and the results prompted changes in previously described methods. All specimens were very carefully protected from light; extraction and acidification were done with acetic acid instead of hydrochloric acid. With these precautions no 4-chloro-5-sulphamoylanthranilic acid was found in biological specimens. The main metabolite was furosemide glucuronide (20% of furosemide excretion). Sensitivity was 0.1 and 0.5 microgram/ml for plasma and urine, respectively. The applicability of our method for furosemide studies is demonstrated.

Adult↗
PubMed1997

Determination and pharmacokinetics of a furosemide-amiloride drug combination.

The study presents an accurate and precise HPLC assay for the determination of furosemide and amiloride in human specimens. Both drugs were extracted from human plasma with ethyl acetate; furosemide was extracted at pH 1 and amiloride at pH 12. While chromatographic separation conditions, i.e., column, mobile phase and flow-rate were the same for both investigated drugs, furosemide was detected using a UV absorbance detector, whereas amiloride, because of its very low therapeutic range, was detected with a spectrofluorimetric detector. The linearity of the furosemide and amiloride assays were confirmed over the range of 30-3000 ng/ml and 0.5-30 ng/ml, respectively. These concentrations correspond well with the therapeutic ranges of both drugs. The extraction recoveries, depending on concentration, exceed 80% for furosemide and 74% for amiloride. The reported methods were applied to pharmacokinetic investigations of the two compounds taken in form of a drug combination.

Adult↗
PubMed1998

High-performance liquid chromatographic determination of furosemide in plasma and urine and its use in bioavailability studies.

A sensitive, selective and efficient reversed-phase high-performance liquid chromatographic (HPLC) method is reported for the determination of furosemide in human plasma and urine. The method has a sensitivity limit of 5 ng/ml in plasma, with acceptable within- and between-day reproducibilities and good linearity (r2>0.99) over a concentration range from 0.05 to 2.00 microg/ml. The one-step extract of furosemide and the internal standard (warfarin) from acidified plasma or urine was eluted through a muBondapak C18 column with a mobile phase composed of 0.01 M potassium dihydrogenphosphate and acetonitrile (62:38, v/v) adjusted to pH 3.0. Within-day coefficients of variation (C.V.s) ranged from 1.08 to 8.63% for plasma and from 2.52 to 3.10% for urine, whereas between-day C.V.s ranged from 4.25 to 10.77% for plasma and from 5.15 to 6.81% for urine at three different concentrations. The minimum quantifiable concentration of furosemide was determined to be 5 ng/ml. The HPLC method described has the capability of rapid and reproducible measurement of low levels of furosemide in small amounts of plasma and urine. This method was utilized in bioavailability/pharmacokinetic studies for the routine monitoring of furosemide levels in adults, children and neonate patients.

Biological Availability↗
PubMed2001

Furosemide alters nonlinear capacitance in isolated outer hair cells.

The outer hair cell (OHC) from the organ of Corti plays a crucial role in hearing through its unique voltage-dependent mechanical responses. Furosemide, one of the loop diuretics, disrupts normal cochlear function. Here we report on direct effects of furosemide on OHC motility-related, voltage-dependent capacitance using the whole-cell patch-clamp technique. Extracellularly applied furosemide reversibly shifted the voltage at peak capacitance (V(pkC(m))) to positive levels. The shift, whose maximum approached 90 mV, evidenced a Hill coefficient of 1.5 and K(1/2) of 10 mM. Changes in the magnitude of nonlinear capacitance were not fully reversible. While it is clear that the overwhelming effect of furosemide on hearing results via its effects on the endolymphatic potential, the present results indicate that furosemide directly alters OHC motility and may, in part, contribute to sensory dysfunction.

Animals↗
PubMed1993

Pharmacokinetics of furosemide in endolymph.

To investigate the pharmacokinetics of organic anions in the endolymph of the guinea pig, 100 mg/kg furosemide, an organic anion, was intravenously given to measure the concentration in the cochlear endolymph by high-performance liquid chromatography with fluorescence detection. In the endolymph, the concentration of the furosemide increased slowly for 1 hr to 1.6 micrograms/ml and gradually declined thereafter. Pretreatment with 200 mg/kg probenecid, an anion transport inhibitor, had no effect on the furosemide elimination in the endolymph except on the concentration at 2 hr. This was contrary to the drastic change observed in the perilymph of the scala tympani by the same pretreatment. Analogous to the effect in the endolymph, probenecid showed no change in the concentration of the serum, while a pronounced gradient of furosemide concentration existed between them. The present results suggest that the furosemide passively transfers from blood to the endolymph at a relatively low penetrability.

Animals↗
PubMed2000

Furosemide assay in pharmaceuticals by Micellar liquid chromatography: study of the stability of the drug.

A simplified high-performance liquid chromatographic procedure is described for the determination of furosemide (4-chloro-N-furfuryl-5-sulphamoylanthranillic acid), which makes use of UV detection, a C18, reversed-phase column, and micellar mobile phases of sodium dodecyl sulphate (SDS) and 1-propanol at pH 3 buffered with phosphate system. The most adequate experimental conditions to handle furosemide solutions in the analytical laboratory are studied. The mixture of furosemide and its degradation products which are formed upon light exposition was resolved with a mobile phase of 0.04 M SDS-2% propanol. Separation of furosemide from its common impurities and the hydrolytic product, 4-chloro-5-sulphamoylanthranillic acid, was also possible. A mobile phase of larger elution strength, such as 0.06 M SDS-8%, propanol was preferred to assay furosemide in several dosage forms (tablets, capsules, injectables and drops). The validity of the procedure was checked by analysing 27 pharmaceuticals commercialised in several countries. The label claim percentages and coefficients of variation were in the 95-102% and 0.05-1.3% ranges, respectively. The results showed that the procedure is suitable for routine analysis of the diuretic.

Calibration↗
PubMed2003

Torasemide vs. furosemide in primary care patients with chronic heart failure NYHA II to IV--efficacy and quality of life.

BACKGROUND: The hypothesis was that torasemide, due to more predictable pharmacokinetics/pharmacodynamics, induces greater improvements in functional and social limitation than furosemide and reduces the frequency of hospitalisations in primary care patients with chronic heart failure (CHF). PATIENTS AND METHODS: Prospective, randomized, unblinded study in primary care, 237 patients with CHF (NYHA II-IV), all on ACE inhibitors. Randomisation: torasemide (n=122) or furosemide (n=115), treated for 9 months. ENDPOINTS: Clinical efficacy, quality of life, safety, tolerability, hospitalisations. RESULTS: Clinical improvement was observed in both groups, but the trend to improve by at least one NYHA class was significant only in torasemide- (P=0.014), but not in furosemide-treated patients. There were no differences with regard to adverse events and hospitalisation due to CHF. Overall, tolerability (P=0.0001) and improvement in daily restrictions (P=0.0002) were significantly higher, number of mictions at 3, 6 and 12 h after diuretic intake (P<0.001 at all time points) and urgency to urinate (P<0.0001) significantly lower in torasemide- vs. furosemide-treated patients. CONCLUSION: CHF patients treated with torasemide gain a higher benefit in quality of life than furosemide treated patients, due to torasemide's dual effect on both clinical status and social function.

Aged↗
PubMed2003

Impact of Mrp2 on the biliary excretion and intestinal absorption of furosemide, probenecid, and methotrexate using Eisai hyperbilirubinemic rats.

PURPOSE: This study assesses the impact of rat multidrug resistance-associated protein 2 (Mrp2) on the biliary excretion and oral absorption of furosemide, probenecid, and methotrexate using Eisai hyperbilirubinemic rats (EHBR). METHODS: To assess Mrp2-mediated biliary excretion, rats received a 2-h intravenous infusion of furosemide, probenecid, or methotrexate. Blood and bile samples were collected at specified intervals. To assess Mrp2's impact on oral absorption, rats received furosemide, probenecid, or methotrexate orally at 5 mg/kg. Jugular and portal blood samples were obtained at timed intervals. All samples were analyzed by LC-MS/MS. Pharmacokinetic parameters were estimated using WinNonlin and standard pharmacokinetic equations. RESULTS: Thirty seven- and 39-fold reductions in biliary clearance were observed in EHBR as compared to control rats for probenecid and methotrexate, respectively. Biliary clearance was comparable between EHBR and control rats for furosemide. In all cases, no significant difference in absorption was observed between EHBR and control rats. CONCLUSIONS: This study provides the first evidence that Mrp2 mediates the biliary excretion of probenecid but not furosemide. Additionally, Mrp2 apparently has a less profound impact on intestinal absorption than biliary excretion of its substrates. Furthermore, alteration in systemic clearance in EHBR indicates that a potential compensatory mechanism may occur in EHBR.

ATP-Binding Cassette Transporters↗
PubMed1980

Comparison of oral indacrinone with furosemide.

The oral dose response and time course of action of indacrinone was compared with that of furosemide in six healthy men on a sodium and potassium-controlled diet. The single doses were 5, 10, 20, 40, and 80 mg indacrinone and 20, 40, and 80 mg furosemide. Diuretic, natriuretic, and kaliuretic effects revealed that indacrinone was more potent, had a longer duration of action, and induced a greater sodium for equivalent potassium loss during its period of peak activity than furosemide. During the 8 hr after drug, all doses of indacrinone decreased serum uric acid levels and increased uric acid clearance while furosemide generally increased serum uric acid and decreased uric acid clearance. After 24 hr, serum uric acid and uric acid clearance were the same for the two drugs. A rise in plasma renin activity was observed 2 hr after an 80-mg dose of furosemide but not after indacrinone.

Adult↗
PubMed1981

Effect of ouabain and furosemide on erythrocyte sodium and phosphate transport.

The effects of ouabain and furosemide on the unidirectional efflux of sodium and phosphate ions were studied in freshly drawn human red blood cells (RBCs). In the presence of physiologic concentrations of sodium and potassium the rate of sodium efflux was reduced by 74% due to ouabain sensitivity. Furosemide (1.0 mmol/l) reduced ouabain-insensitive sodium transport rate by a further 50%. Thus, 13% of total sodium efflux was inhibited by furosemide when ouabain was present. In the absence of ouabain, however, furosemide inhibited 31% of total sodium transport, indicating that it also affected ouabain-sensitive sodium efflux. Phosphate transfer of RBCs was almost 1.0 mmol/l RBCs per hour. Erythrocyte concentration of orthophosphate, however, was only 0.59 mmol/l RBCs. Organic phosphate esters must therefore have been cleaved to maintain constant phosphate elimination. The hydrolysis of adenosine triphosphate (ATP) by Na-K-ATPase might be involved because the phosphate transfer of almost 0.12 mmol/l RBCs per hour was ouabain sensitive. Furosemide reduced phosphate efflux by 50% due to reduction in passive permeability of the RBC membrane. Additional inhibition of any phosphate ester hydrolyzing enzymatic activity cannot, however, by excluded.

Adult↗
PubMed1981

Prevention of cyclophosphamide-induced antidiuresis by furosemide infusion.

In patients receiving high-dose cyclophosphamide therapy (HDCPT), urinary flow rate, serum sodium concentration, and renal free-water clearance frequently decrease in the 24 hr after drug. High urinary flow rates, which may minimize other cyclophosphamide-related symptoms, are difficult to achieve in the face of the antidiuretic effect. Five patients receiving a total of 30 doses of HDCPT (greater than 50 mg/kg) were studied to assess the effect of continuous furosemide infusion on cyclophosphamide antidiuresis. In two patients receiving various diuretic regimens, only the continuous infusion of furosemide was associated with maintenance of high urinary flow rates and normal serum sodium concentrations. Four patients studied prospectively while receiving HDCPT maintained renal free-water clearance as well as high constant urinary flow rates and normal serum sodium concentrations. Concurrent studies of furosemide disposition revealed that renal excretion of furosemide was unchanged during the continuous infusion and that the diuretic effect was sustained throughout the therapeutic course. The only furosemide-related side effect identified was hypokalemia, which was easily managed with potassium chloride given intravenously.

Adolescent↗
PubMed1982

Furosemide disposition in cirrhosis.

Furosemide disposition after rapid intravenous injection (80 mg) was studied in 10 normal healthy subjects and eight patients with cirrhosis and ascites. In the cirrhotic patients the elimination half-life was modestly longer (81.0 +/- 8.0 min and 60.2 +/- 5.8 min). This prolongation was not associated with a difference in systemic clearance (156 +/- 7 ml/min in normal and 142 +/- 16 ml/min in cirrhotic subjects), rather it was a reflection of alterations in furosemide distribution. The steady-state volume of distribution was increased from 8.5 +/- 0.4 l in the healthy subjects to 12.1 +/- 1.3 l in the cirrhotic subjects; estimation in terms of unbound drug indicated an approximately 50% smaller value in cirrhosis. These observations were quantitatively consistent with the increased percentage of furosemide in plasma in the unbound form in the patients (10.2 +/- 1.0%) compared to in the normal subjects (4.0 +/- 0.1%). The 24-hr percentage urinary recovery of unchanged drug (58.8 +/- 2.8% and 53.1 6.5%) and the glucuronide metabolite (17.8 +/- 1.5 and 21.3 +/- 3.4) were on the same order in the normal and cirrhotic groups. The lack of major effects of cirrhosis on furosemide disposition suggests that changes in furosemide diuretic efficacy in such patients is a result of altered dynamic factors rather than altered disposition.

Adult↗
PubMed1986

Furosemide kinetics and dynamics in patients with cirrhosis.

Factors that influence intersubject variability in response to furosemide have been investigated in normal subjects and patients with cirrhosis. Furosemide pharmacokinetics and pharmacodynamics were measured in eight normal subjects and 14 patients with cirrhosis, eight of whom were resistant to diuretic therapy. Furosemide renal clearance decreased in proportion to creatinine clearance, whereas nonrenal clearance and volume of distribution were unchanged. These pharmacokinetic changes were, however, minimal and resulted in an only marginal alteration in the plasma concentration-time curve. The maximal rate of urinary sodium excretion decreased with reductions in creatinine clearance (r = 0.77). However, the extent of reduction in urinary excretion of sodium was proportionally greater than the reduction in creatinine clearance, whereas the rate of urinary furosemide excretion required to achieve 50% of maximal response did not change. Furosemide's pharmacokinetics were not, therefore, appreciably altered by cirrhosis. However, cirrhosis was associated with a reduction in pharmacodynamic response to this diuretic.

Adult↗
PubMed1984

Bumetanide and furosemide in heart failure.

We assessed the handling of and response to oral bumetanide (1.0 and 2.0 mg) and to furosemide (40 and 80 mg) in 20 patients with stable, compensated congestive heart failure (CHF), comparing the two drugs and, in addition, examining differences from normal subjects. Bumetanide and furosemide were similar in time course of absorption, but patients with CHF had considerably prolonged absorption compared to normal subjects causing attainment of lower peak concentrations of drug. In both CHF and normal subjects, more bumetanide than furosemide was absorbed. The elimination half-life of furosemide was approximately twice that of bumetanide, and both were about two times longer than respective values in normal subjects. "Dose"-response curves were shifted downward from normal with both drugs. In patients with CHF, overall response did not differ between bumetanide and furosemide. The two drugs exhibit subtle differences, the clinical importance of which appears to be negligible from this study. Importantly, however, both drugs showed delayed absorption causing attainment of peak urinary excretion rates of diuretic two- to threefold lower than in normal subjects. This effect along with the abnormal responsivity of the tubule may contribute to the "resistance" to oral doses of diuretics observed clinically even though no quantitative malabsorption of drug occurs.

Absorption↗
PubMed1997

Furosemide-induced changes in plasma and blood volume of camels (Camelus dromedarius).

This work examines the effect of treatment of camels with furosemide (1 or 2 mg/kg, intravenously) on blood volume (BV), plasma volume (PV) and the plasma concentrations of total solids (PTS), plasma total protein (PTP) haemoglobin (Hb) and haematocrit (PCV). The cumulative urine produced during the 4 h following furosemide administration (2 mg/kg) averaged 22.2 mL/kg, compared to 2.3 mL/kg in controls. None of the above parameters were significantly changed by furosemide treatment at either dose. In another experiment, the effect of the two doses of furosemide on the sequential changes on some of the above parameters was investigated at 5, 10, 15, 30, 45, 60, 75, 90, 105, 120 and 240 min after the drug administration. On the whole, there were no significant changes in any of the measured parameters, except for small but statistically significant increases in the PCV and Hb at 30 and 45 min post treatment. It is concluded that, despite the marked diuresis following furosemide administration, the camel appears to be able to maintain its bodily fluid haemostasis.

Animals↗
PubMed1998

The pharmacokinetics of furosemide in anaesthetized horses after bilateral ureteral ligation.

The pharmacokinetics of furosemide were investigated in anaesthetized horses with bilateral ureteral ligation (BUL) with (n = 5) or without (n = 5) premedication with phenylbutazone. Horses were administered an intravenous (i.v.) bolus dose of furosemide (1 mg/kg) approximately 60-90 min after BUL. Plasma samples collected up to 3 h after drug administration were analysed by a validated high performance liquid chromatography method. Median plasma clearance (CLp) of furosemide in anaesthetized horses with BUL was 1.4 mL/min/kg. Apparent steady state volume of distribution (Vd(ss)) ranged from 169 to 880 mL/kg and the elimination half life (t1/2) ranged from 83 min to 209 h. No differences in plasma concentration or kinetic parameter estimates were observed when phenylbutazone was administered before furosemide administration. BUL markedly reduces the elimination of furosemide in horses and models the potential effects that severe changes in kidney function may have on drug kinetics in horses.

Animals↗
PubMed2002

Furosemide and 11beta-hydroxysteroid dehydrogenase activity, in man.

Mineralocorticoid receptors possess the same affinity for aldosterone and for cortisol and preferential binding of aldosterone is modulated by the 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) enzyme, which converts cortisol to its inactive metabolite cortisone. Several endogenous or exogenous compounds able to inhibit the enzyme have been described and, as a consequence, produce the syndrome of apparent mineralocorticoid excess (AME) characterized by hypertension, hypokalemia, volume repletion and suppression of the renin-angiotensin-aldosterone system. High doses of furosemide, a diuretic that works in the luminal surface of the thick ascending limb of Henle's loop, have been reported to inhibit 11 beta-OHSD activity to the same extent as licorice in vivo and in vitro, in rat. The aim of our study was to verify the effect of the drug on 11 beta-OHSD activity in man at the doses currently used in clinical practice. We tested the activity of 11 beta-OHSD following both acute and protracted administration of furosemide. In the acute study, the drug was administered at low (40 mg i.v. in bolo) and high doses (infusion of 10 mg/kg bw i.v for six hours); the protracted furosemide administration consisted in 50 mg/day for 20 days, by mouth. The ratios between the cortisol metabolites tetrahydrocortisol plus allo-tetrahydrocortisol to tetra-hydrocortisone and urinary free cortisol to urinary free cortisone were used to measure the activity of 11 beta-OHSD. Urinary cortisol, cortisone and their metabolites were tested by a gas-chromatographic/mass spectrometric method. Neither acute nor prolonged administration of furosemide did affect the activity of 11 beta-OHSD although the drug was able to modify plasma aldosterone and PRA secretion and to determine hypokalemia. Our results suggest that furosemide does not play a significant role in 11 beta-OHSD modulation in humans, at least at the dosage used in clinical practice.

11-beta-Hydroxysteroid Dehydrogenases↗