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PubMed1991

Pharmacokinetic, biliary excretion, and metabolic studies of 14C-furosemide in the rat.

1. Partition of furosemide into organic solvents at pH 3.8 was greatest for ethyl acetate (33:1) greater than 2-ethyl-1-hexanol (10:1) greater than ethyl ether (6:1). 2. Furosemide was highly bound to human, bovine, rabbit, and rat plasma or albumin (97.4-98.4%). 3. Furosemide was highly bound to rat tissues. One hour after i.p. injection of the drug, tissue to plasma concentration ratios were: adrenals (10:1), lung (4:1), kidney (4:1), spleen (3:1). 4. In rats with ligated renal pedicles, furosemide was excreted in bile, at least in part, by active transport. Hepatic clearance of a 1 mg/kg i.v. dose contributed 20% to total body clearance. Large doses (50 mg/kg and more) of furosemide exerted a choleretic effect. 5. Chromatography of bile showed that i.v. administration of 50 mg/kg and higher doses of furosemide to rats resulted in saturation of hepatic drug metabolism. 6. The bile of rats contained the parent drug, 4-chloro-5-sulphamoyl-anthranilic acid, and at least two unknown metabolites with the furan ring intact.

Adrenal Glands↗
PubMed1975

Effects of indomethacin on furosemide-induced changes in renal blood flow.

The effects of indomethacin on furosemide induced changes in renal blood flow were determined in dogs. Furosemide alone caused an increase in total renal blood flow while indomethacin alone decreased renal blood flow. When furosemide was administered to animals pretreated with indomethacin the increase in renal blood flow was blocked. Changes in intrarenal blood flow distribution were also measured using radioactive microspheres. The pattern of blood flow distribution after furosemide was modified in some of the animals pretreated with indomethacin. Stimulation of renin secretion occurred after furosemide in indomethacin-treated animals. The data suggest that the changes in renal blood flow produced by furosemide may be modulated by the prostaglandin system.

Animals↗
PubMed1995

[Evaluation of the furosemide test using the air caloric stimulator].

Both the furosemide test, and the glycerol test have been reported as being effective for detection of endolymphatic hydrops. In the furosemide test, the caloric test is performed first, and then repeated 40 minutes after i.v. injection of furosemide, 20 mg. The maximum velocities of each caloric nystagmus are compared, so the caloric stimulus conditions must be constant. In the original method, the caloric test is performed by irrigation with 50 ml of water at 30 degrees C or 44 degrees C for 20 seconds. Since it is difficult to accurately maintain the water temperature at a constant level, however, we use the air caloric stimulator NCA-105 (ICS) for the furosemide test. By using this stimulator, we can always perform the caloric test under the same conditions. The conditions of air irrigation in 28 normal subjects were set at 37 +/- 11 degrees C, 61/min, and 60 seconds. These conditions were confirmed in other normal subjects to fairly well correspond to water irrigation (30 degrees C or 44 degrees C, 50 ml, 20 seconds). Next we reassessed the furosemide test by using the air caloric stimulator in normal subjects. As a result, positive effects were observed in 7.4% of the normal subjects. This finding was similar to that reported in the literature (Futaki et al., 1971). The air caloric test is considered to be a more useful examination than the water caloric test because it is less unpleasant for the subject and easily provides the same conditions before and after furosemide administration.

Adolescent↗
PubMed1985

Furosemide absorption altered in decompensated congestive heart failure.

We assessed whether patients with decompensated congestive heart failure had altered absorption of oral furosemide. Pharmacokinetic and pharmacodynamic responses were studied in 11 patients receiving their usual oral dose of furosemide while decompensated, and after attaining normal weight. Seven patients also received 25 g of oral D-xylose to further assess intestinal absorption. A 57% decrease in lag time (p = 0.033), a 27% decrease in time to peak serum concentration (p = 0.041), and a 29% increase in the peak serum furosemide concentration (p = 0.008) were seen in compensated as compared to decompensated patients. No significant change was seen in absorption or elimination half-lives, area under the serum concentration versus time curves for furosemide, or in absorption of D-xylose. Although the pharmacodynamics of furosemide were reduced compared to normal subjects, there was little difference in the compensated and decompensated states. Our results show an alteration in furosemide absorption in decompensated congestive heart failure.

Adult↗
PubMed1976

[Platelet anti-aggregating activity of furosemide (author's transl)].

The effect of furosemide on platelet aggregation, factor 3 availability, and response to hypotonic stress has been studied. Furosemide greatly inhibits platelet aggregation, with ADP, epinephrine, collagen, ristocetin, thrombin and serotonin. The use of heparin as anticoagulant does not alter this effect. Furosemide action is not conducted through calcium chelation. Platelet factor 3 availability is not modified by furosemide. There is a direct correlation between furosemide concentration and inhibition in the second phase of platelet response to hypotonic stress. The possibility of a disorder furosemide induced on the platelet metabolism, is suggested.

Adult↗
PubMed2000

[Nephrotoxicity of piperacillin combined with furosemide in rats].

Nephrotoxicity of piperacillin (PIPC) was evaluated in rats after combined administration with furosemide. After intravenous administration of PIPC (1600 mg/kg), the rats showed no change in urinalysis, biochemical analysis of plasma and histopathological analysis. The rats receiving furosemide (100 mg/kg) showed elevation of urinary NAG, BUN and creatinine concentrations, and showed slight degeneration of the renal proximal tubules. The rats receiving PIPC (1600 mg/kg) and furosemide (100 mg/kg) showed elevation of BUN and creatinine concentrations, and showed slight degeneration of the proximal tubules. These changes were comparable to those in rats receiving furosemide alone. The rats receiving cephaloridine (1600 mg/kg) showed elevation of urinary protein, BUN and creatinine concentrations, and showed moderate degeneration and necrosis of the proximal tubules. The nephrotoxicity was enhanced by combination with furosemide. In conclusion, no enhanced effect of nephrotoxicity was observed by combination of PIPC with furosemide.

Animals↗
PubMed2001

A(1) receptor blockade induces natriuresis with a favorable renal hemodynamic profile in SHHF/Mcc-fa(cp) rats chronically treated with salt and furosemide.

Our goal was to test the hypothesis that A(1) receptor blockade induces diuresis/natriuresis with a favorable renal hemodynamic/cardiac profile in aged, lean SHHF/Mcc-fa(cp) rats, a rodent model of hypertensive dilated cardiomyopathy. Thirteen-month-old SHHF/Mcc-fa(cp) rats were pretreated for 72 h before experiments with furosemide (100 mg/kg by gavage 72, 48, and 24 h before experiments) to mimic the clinical setting of chronic diuretic therapy and were given 1% NaCl as drinking water to reduce dehydration/sodium depletion. Animals were instrumented for measurement of systemic and renal hemodynamics, renal excretory function, and cardiac performance, and baseline values were obtained during a 30-min clearance period. Animals then received either vehicle (n = 9), BG9719 [the S-enantiomer of 1,3-dipropyl-8-[2-(5,6-epoxynorbornyl)] xanthine (also called CVT-124)] (highly selective A(1) receptor antagonist; 0.1 mg/kg bolus + 10 microg/kg/min; n = 9) or furosemide (loop diuretic; 30 mg/kg; n = 8) and measurements were repeated during four subsequent clearance periods. Both BG9719 and furosemide increased urine volume and absolute and fractional sodium excretion. BG9719 increased renal blood flow and glomerular filtration rate, but did not affect fractional potassium excretion. Furosemide decreased renal blood flow and glomerular filtration rate and increased fractional potassium excretion. Neither drug altered afterload; however, furosemide, but not BG9719, decreased preload (central venous pressure and ventricular end diastolic pressure). Neither drug altered systolic function (+dP/dt(max)); however, furosemide, but not BG9719, attenuated diastolic function (decreased -dP/dt(max), increased tau). In the setting of left ventricular dysfunction, chronic salt loading and prior loop diuretic treatment, selective A(1) receptor antagonists are effective diuretic/natriuretic agents with a favorable renal hemodynamic/cardiac performance profile.

Animals↗
PubMed1976

Effect of experimental azotemia on renal clearance of furosemide in the dog.

The clearance of furosemide (F), whose renal tubular transport shares the classical characteristics of the organic acid system, was determined in dogs with varying degrees of azotemia and compared with tetraethylammonium (TEA), an organic base. Two normal and eight azotemic dogs [blood urea nitrogen (BUN), 12-273] were studied. Azotemia was produced by bilateral uretero-venous anastomoses. The left renal vein and ureter were cannulated and renal blood flow (RBF) was measured by electromagnetic flowmeter. Simultaneous left renal clearances (C) of subpharmacological doses of TEA-14C and furosemide-14C were determined at seven 30-minute intervals. Initial loading doses were followed by continuous maintenance infusions. For TEA, clearance (1.5 ml/min-g +/- 0.2 S.E.M.) and extraction (E) (0.83 +/- 0.02) are independent of the degree of azotemia. Renal plasma flow (RPF), calculated as CTEA/ETEA, agreed closely with directly measured RPF (2.0 ml/g-min +/- 0.3). RPF was independent of azotemia. To allow for individual differences in the animals in RPF, the ratio CTEA/CF was used. CF (1.07-0.17 ml/min-g) and EF (0.54-0.06) decreased as a linear function of the increase in uremic serum: (see article). Furosemide and its principle metabolite were greater than or equal to 97% of the furosemide portion of the radioactivity. The metabolite did not increase with time in either plasma or urine. After acute administration of exogenous urea to two dogs (BUN 170 and 253) CTEA/CF was unrelated to BUN. Thus, the CF decreases proportionately with progressive azotemia and is not related to RBF, exogenous urea or metabolite. This suppression of renal tubular secretion of furosemide may partially account for reduced therapeutic efficacy of furosemide in azotemia.

Animals↗
PubMed2003

Thiamine deficiency in congestive heart failure patients receiving long term furosemide therapy.

OBJECTIVE: To assess the presence of thiamine deficiency in congestive heart failure patients receiving furosemide therapy. DESIGN: Prospective, biochemical analysis of thiamine status was performed in outpatients and inpatients of the University of Ottawa Heart Institute. SUBJECTS: Thirty-two patients with congestive heart failure who received at least 40 mg/day of furosemide were included. Patients were then separated into two groups depending on whether the dose of furosemide was greater than or equal to 80 mg/day. METHODS: The primary measure was actual thiamine status as assessed by the erythrocyte transketolase enzyme activity and the degree of thiamine pyrophosphate effect. RESULTS: Biochemical evidence of severe thiamine deficiency was found in 98% (24 of 25) patients receiving at least 80 mg/day of furosemide and in 57% (four of seven) of patients taking 40 mg furosemide daily, odds ratio (OR) 19.0 (1.13<OR<601.29). Thiamine status was not associated with any other clinical variables. CONCLUSIONS: These findings suggest that thiamine deficiency occurs in a substantial proportion of congestive heart failure patients being treated with furosemide.

Aged↗
PubMed1992

Development of absorption furosemide prodrugs: synthesis, in vitro and in vivo evaluation.

Six acyloxymethyl esters of Furosemide were synthesized and the structures were determined by chemical and spectroscopic methods. Lipophilicity parameters were analysed by high performance liquid chromatography (HPLC). Hydrolysis performances in human plasma and intestinal fluids anticipate their properties as absorption prodrugs of Furosemide. A bioavailability study carried out with 8 male Wistar rats with one of the synthesized prodrug (acetyloxymethyl 4-chloro-N-furfuryl-5-sulfamoylanthranilate) showed a greater absorption in relation to Furosemide. The percentages of mean urinary recovery of Furosemide for the prodrug and for the standard solution of the drug were 20.84 and 14.36 respectively. The doses were 10 mg/Kg in Furosemide. The analytical determinations of Furosemide in biological fluids were done by HPLC.

Animals↗
PubMed1992

Cholelithiasis in infants receiving furosemide: a prospective study of the incidence and one-year follow-up.

Cholelithiasis has been reported to occur rarely in infants. To determine the incidence of cholelithiasis in infants receiving furosemide, we prospectively performed ultrasonograms on 86 patients. We studied 42 patients receiving furosemide (subjects) and 44 patients not receiving furosemide (controls). There was a significantly higher incidence of gallstones in subjects (21%) than in controls (2%) (P less than .05). When followed over 1 year, the gallstones did not resolve. There were no significant differences in the dosage of furosemide, gestational age, placement of umbilical venous catheters, or amount of total parenteral nutrition (TPN) between subjects with and without gallstones. However, subjects received more days of TPN (16.7 +/- 15.1) than controls (8.4 +/- 13.2) (P less than .05). These data show that the incidence of cholelithiasis is higher than previously suspected in infants receiving furosemide. Thus, furosemide, either independently or in conjunction with the use of TPN, predisposes infants to the development of cholelithiasis.

Bronchopulmonary Dysplasia↗
PubMed2004

High-dose furosemide for established ARF: a prospective, randomized, double-blind, placebo-controlled, multicenter trial.

BACKGROUND: The effect of furosemide on the survival and renal recovery of patients presenting with acute renal failure (ARF) is still debated. METHODS: Three hundred thirty-eight patients with ARF requiring dialysis therapy were randomly assigned to the administration of either furosemide (25 mg/kg/d intravenously or 35 mg/kg/d orally) or matched placebo, with stratification according to severity at presentation. The primary end point was survival. The secondary end point was number of dialysis sessions. Tertiary end points included time on dialysis therapy, time to achieve a serum creatinine level less than 2.26 mg/dL (<200 micromol/L), and time to reach a 2-L/d diuresis. RESULTS: There were no differences in survival and renal recovery rates between the 2 groups. Time to achieve a 2-L/d diuresis was shorter with furosemide (5.7 +/- 5.8 days) than placebo (7.8 +/- 6.8 days; P = 0.004). Overall, 148 patients achieved a urine output of at least 2 L/d during the study period (94 of 166 patients; 57%) with furosemide versus 54 of 164 patients (33%) with placebo ( P < 0.001). However, there were no significant differences in number of dialysis sessions and time on dialysis therapy between the furosemide and placebo groups, even in the subgroup of patients reaching a 2-L/d diuresis. CONCLUSION: High-dose furosemide helps maintain urinary output, but does not have an impact on the survival and renal recovery rate of patients with established ARF.

Acute Kidney Injury↗
PubMed2004

Urinary fluorine-18 fluorodeoxyglucose excretion with and without intravenous application of furosemide.

METHODS: Twenty patients suffering from malignancy received furosemide, twenty patients were examined by FDG-PET without diuretics. Urine volume and radioactivity were measured before and after acquisition. Bladder activity was evaluated qualitatively and quantitatively. RESULTS: Radioactivity in the bladder was lower and the image quality higher in the furosemide group. SUV values showed a median of 3.0 in the furosemide and 6.0 in the control group. With furosemide, a larger excreted volume was seen compared to the control group. The furosemide group showed a significantly higher ratio of excreted/ injected radioactivity early after injection. However, the totally excreted radioactivity was not significantly different (p = 0.93). CONCLUSION: Diuretics cause a higher urine volume with a diluted FDG concentration leading to an improved image quality. Furosemide accelerates early renal FDG elimination, reducing radiation exposure.

Diuretics↗
PubMed1992

Diuretic and non-diuretic actions of furosemide: effects of probenecid.

Furosemide causes not only natriuresis, but a rapid (5-10 min) increase in plasma renin activity. The latter has been attributed both to the release of eicosanoids from renal blood vessels and to changes in sodium delivery to the macula densa. Drugs like indomethacin abolish the renin increment and could potentially affect both mechanisms: they inhibit cyclooxygenase but could also compete with furosemide for transport into the tubular lumen, reducing furosemide concentration at its site of action. We studied the effects of probenecid, a weak acid without cyclooxygenase activity, on the responses to furosemide in 20 healthy young men. Each received placebo and low (1000 mg/d) or high (2000 mg/d) doses of probenecid for one week in double-blind, randomized trials, crossover fashion. One hour after the last dose, all participants were given furosemide 0.5 mg/kg intravenously. Probenecid reduced serum uric acid in a dose-dependent manner but did not change platelet thromboxane B2 production. Similarly, there was no change in urine excretion rates of thromboxane B2 or 6ketoprostaglandin F1 alpha, or in baseline or stimulated plasma renin activity. The total natriuresis in 4 h was also unchanged. By contrast, the sodium excretion rate in the first 30 min was reduced after both probenecid regimens while that of later periods was increased. These findings are consistent with the proposed effect of probenecid as reducing furosemide secretion in the proximal tubule, which reduces its concentration at the lumenal surface of the thick ascending limb of Henle's loop, but also prevents its excretion from the body.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

Furosemide use and hospitalization for benign prostatic hyperplasia.

OBJECTIVE: Recent studies have shown that furosemide may have anti-inflammatory properties. We explored whether exposure to furosemide would reduce the risk of being hospitalized with prostatism, a marker of benign prostatic hyperplasia. METHODS: Using record linkage and the computerized health insurance databases of the province of Québec, Canada, we identified a cohort of men 65 years of age and older within which we conducted a case-control study. Cases were individuals hospitalized with prostatism (ICD-9 code 600) between January 1991 and June 1993, with the index date taken as the date of hospitalisation. Controls were those not having experienced the event during the study period, with an index date selected randomly during their follow-up. Cases and controls were required to have at least 2 (1/2) years of health coverage prior to index date in order to identify risk factors for benign prostatic hyperplasia and establish baseline medical history. We assessed the subjects' exposure to furosemide and various other diuretics in the period 180 to 900 days preceding the index date. Logistic regression was used to evaluate the association between the use of furosemide and hospitalization for prostatism, adjusting for potential confounders. RESULTS: The cohort included 8,814 subjects, of which 231 were cases and 8,583 controls. The rate of hospitalization for prostatism was lower for users of furosemide compared to non-users (adjusted rate ratio 0.49; 95% CI: 0.25-0.95). There was no association with the use of thiazide or potassium sparing diuretics (adjusted rate ratio 0.95; 95% CI: 0.65-1.37). Results suggestive of a protective effect associated with corticosteroid use were observed (adjusted rate ratio 0.64; 95% CI: 0.44-0.93). CONCLUSIONS: This study supports the hypothesis that furosemide can reduce the risk of hospitalization for prostatism, a marker of benign prostatic hyperplasia.

Case-Control Studies↗
PubMed2006

Intravenous furosemide injection during 18F-FDG PET acquisition.

UNLABELLED: Urinary-system elimination of (18)F-FDG can be mistaken for pathologic uptake. Furosemide helps eliminate this artifact. Unnecessary administration should be avoided. Our approach obviates furosemide administration and other invasive procedures in many cases. METHODS: Thirty-seven cancer patients referred for PET to evaluate treatment response or suspected recurrence were prospectively studied using whole-body scanning, with (18)F-FDG injected via dorsal hand catheter beforehand. The catheter was left in place to enable injection of furosemide while the patient was inside the scanner. After abdominopelvic scanning, physicians evaluated the need to inject furosemide. Thirty minutes after furosemide injection, another abdominopelvic scan was obtained to detect postinjection urinary tract changes. RESULTS: Postfurosemide images showed effects due to physiologic elimination in 24 patients (64.9%), of whom 11 patients (45.8%) had more than one inconclusive prefurosemide finding. In 13 patients (35.1%), delayed images confirmed persistent lymph node uptake, including 3 patients (23.1%) with 1 lesion. CONCLUSION: Furosemide injection during scanning reduces artifacts, shortens examinations, and helps avoid invasive procedures.

Abdominal Neoplasms↗
PubMed1991

[Urinary acidification by furosemide test].

The aim of this study was to investigate the effect of furosemide on urinary acidification in 7 healthy children (aged 7 to 9 years) 5 patients with normokalemic distal renal tubular acidosis (RTA) (aged 4 to 13 years) and in 1 patient with proximal RTA (aged 20 months). Furosemide was given (2 mg/kg orally) as a tool to stimulate H+ and K+ secretion by enhancing Na delivery and transport in distal tubular segments. Patients with distal RTA were diagnosed by means of the ammonium chloride test and the alkaline overload and the one with proximal RTA by the ammonium chloride test only. Urinary acidification was evaluated 1 hour before and until 4 hours after furosemide administration. Healthy children (Fig. 1) showed a significant fall in urinary pH, 5.8 +/- 0.27 to 4.88 +/- 0.18 (p less than 0.02) and increase of NH3 excretion from 38.58 +/- 10.33 to 79.09 +/- 10.38 microEq/min/1.73 m2 (p less than 0.05). There was a direct correlation between urinary pH and urinary flow: r = 0.62 p less than 0.01 (Fig. 3). In patients with distal RTA (Fig. 5) furosemide failed to lower urine pH below 6 and net acid excretion persisted low: 47.9 +/- 6.1 microEq/min/1.73 m2. In the patient with proximal RTA (Fig. 4) furosemide produced the same effect as in healthy children with a fall in urine pH to 4.4 and an increase in net acid excretion to 118 microEq/min/1.73 m2. Furosemide proved to be effective to differentiate the type of RTA.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗
PubMed1991

Chronotherapeutic study of furosemide in hypertensive subjects: a preliminary report.

In the present study, circadian influences of furosemide on serum electrolytes, lipids and glucose were evaluated in ten hypertensive subjects. A retard capsule (40 mg) of furosemide was given once a day in the morning (07 h 00) or in the evening (19 h 00) for eight weeks. The study was done through a cross-over design. Twenty-four hour urine was collected, and fasting blood samples were obtained during the control period and at the end of each treatment period. The 24-hour urine volume was slightly increased by the repeated administration of furosemide in the morning and evening trials. Urinary excretion of sodium also slightly increased in the morning trial and significantly increased in the evening trial. Serum concentrations of potassium and chloride decreased, while serum uric acid and triglyceride were increased by furosemide treatment. No significant difference was observed in these parameters between morning and evening trials. Fasting blood glucose increased following furosemide. The increment in this parameter was greater in the evening trial than in the morning trial. These findings indicated that the influence of furosemide on glucose tolerance might vary with its time of administration.

Adult↗