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At least 19 recordsLinked to original sources

PubMed2000

Furosemide for symptomatic patent ductus arteriosus in indomethacin-treated infants.

BACKGROUND: Inhibition of prostaglandin synthesis mediates closure of the ductus arteriosus and renal side effects after indomethacin administration. Because furosemide increases prostaglandin production, it could potentially help prevent indomethacin-related toxicity but also decrease ductal response to indomethacin. OBJECTIVES: The primary objectives of this review were to assess (1) whether furosemide affects the incidence of failure of ductal closure after indomethacin and that of indomethacin-related toxicity and (2) the effect of furosemide on mid-term and long-term outcome. The secondary objective was to determine whether the effect of furosemide on renal function and water balance depends on prior extracellular volume (assessed by blood urea nitrogen [BUN]/creatinine ratio). SEARCH STRATEGY: We searched electronic databases (Medline, Embase and Cochrane) and selected abstract books, without language restriction. SELECTION CRITERIA: We selected studies with (1) random allocation to either indomethacin alone or indomethacin and furosemide and (2) analysis of either short-term risk-benefit ratio of furosemide, mid- or long-term outcome, or the relationship between extracellular volume at study entry and changes in renal function. DATA COLLECTION AND ANALYSIS: We assessed studies for possible bias and for quality of assessment of ductal patency. We assessed categorical variables using relative risk and absolute risk reduction. We assessed the effects of furosemide on renal function and fluid balance by comparing changes from baseline in the treatment group with those in controls. Subsets were determined a priori based on BUN/creatinine ratio at study entry. MAIN RESULTS: All 3 studies fulfilling the entry criteria had limitations, including possible or definite bias. There was substantial heterogeneity among studies. Furosemide administration did not significantly increase the risk of failure of ductal closure; however, sample size was insufficient to rule out even a 31% increase. In the subset with initial BUN/creatinine ratio > 20 mg/mg, 2 of 18 patients receiving furosemide could not complete a 3-dose course of indomethacin because of toxicity. Minimal or no information was available about any of the other main outcome variables. Furosemide increased urine output regardless of the initial BUN/creatinine ratio, leading to a 5% weight loss during a 3-dose course, an undesired effect in patients with initial BUN/creatinine ratio > 20 mg/mg. Furosemide increased creatinine clearance only in patients with initial BUN/creatinine ratio <20 mg/mg. REVIEWER'S CONCLUSIONS: There is not enough evidence to support the administration of furosemide to premature infants treated with indomethacin for symptomatic patent ductus arteriosus. Furosemide appears to be contraindicated in the presence of dehydration in those infants.

Cyclooxygenase Inhibitors↗

PubMed2000

Chronic furosemide treatment alters renal responses to furosemide in conscious lambs.

Despite the widespread chronic use of furosemide in the clinical management of a variety of fluid and electrolyte disorders in human infants, the physiological responses to furosemide in the newborn after chronic furosemide treatment are not known. The present experiments were conducted to determine the effects of chronic furosemide treatment on renal responses to acute furosemide challenge in conscious, chronically instrumented lambs. Experiments were carried out on day 1 (before chronic treatment) and on day 7 (after chronic treatment) in lambs given intravenous injections of either furosemide (1 mg/kg per 12 h for 5 days, n=9) or vehicle (0 mg/kg per 12 h for 5 days, n=4). Furosemide-treated animals responded to acute furosemide challenge on day 7 with attenuation of natriuresis and diuresis, and augmentation of kaliuresis compared with responses on day 1. Baseline renin production was elevated, although the renin response to furosemide was similar in chronic furosemide-treated and vehicle-treated lambs. Baseline aldosterone levels were not altered by chronic furosemide treatment, but the aldosterone response to acute furosemide injection was decreased after chronic furosemide treatment. Therefore, chronic furosemide treatment alters renal responses to furosemide in conscious lambs, and alters the aldosterone response to acute furosemide challenge.

Aldosterone↗

PubMed2005

Bucolome, a potent binding inhibitor for furosemide, alters the pharmacokinetics and diuretic effect of furosemide: potential for use of bucolome to restore diuretic response in nephrotic syndrome.

To determine whether bucolome (5-n-butyl-1-cyclohexyl-2,4,6-trioxoperhydropyrimidine), a nonsteroidal anti-inflammatory agent, can reverse diuretic resistance of furosemide in patients with nephrotic syndrome, we examined the inhibitory effect of bucolome on the protein binding of furosemide in serum and urine. Bucolome significantly inhibited the protein binding of furosemide not only in serum but also in urine of preparation albumin (UPA), which mimics urinary albumin concentration in patients with nephrotic syndrome by ultrafiltration method. The binding percentage of furosemide to albumin was approximately 70% in UPA. With coadministration of bucolome to healthy volunteers, renal clearance of furosemide was increased, reflecting the increase of the free fraction of furosemide in serum. Furthermore, coadministration of bucolome caused a significant increase of urine volume and sodium concentration in urine. Even at higher urine levels of furosemide, the inhibitory effect of bucolome on the protein binding of furosemide in UPA remains constant, and changes in pH at weakly acidic pH levels (pH 5.5-6.5) did not alter the inhibitory effect of bucolome. Interestingly, coadministration of bucolome with furosemide in doxorubicin (Adriamycin)-induced nephrotic syndrome model rats alleviated the diuretic resistance. These results suggest that bucolome has a potent inhibitory effect on the protein binding of furosemide in the urine and can partially restore the diuretic response of furosemide in patients with nephrotic syndrome by increasing the free fraction of furosemide at the site of action.

Adult↗

PubMedDate not supplied

Pharmacodynamics and pharmacokinetics of furosemide-retard and furosemide-retard/triamterene.

In a randomized cross-over study the saluretic effect of furosemide-retard was compared with the combination of furosemide-retard/triamterene in 10 healthy male volunteers. The combination led to a significantly stronger excretion of sodium and a significantly lower excretion of potassium than furosemide-retard. The interaction of the saluretic with the antikaliuretic was even more distinctly expressed regarding sodium related quotients. The combination furosemide-retard/triamterene differs significantly from furosemide-retard in the main considering Na+/Cl-, Na+/K+ and Na+/Mg2+ quotients. The concentration time curves for furosemide and OH-TA-sulphate in the plasma are nearly similar. Maximal plasma levels for furosemide are reached after 3.9h and for OH-TA-sulphate after 2.2h. The 'apparent' elimination half-life time for furosemide is 2.1h and the elimination half-life time for OH-TA-sulphate is 2.0h.

Adult↗

PubMed1989

Effect of albumin-bound furosemide on the endocochlear potential of the chinchilla. Alleviation of furosemide-induced ototoxicity.

The effects of albumin-unbound furosemide and albumin-bound furosemide on the cochlear function were compared by the continuous observation of the endocochlear potential (EP) in the chinchilla using the microelectrode method. The EP depression following the intravenous injection of 50 mg/kg of furosemide was 108.5 +/- 2.7 mV, while the addition of 1.0 and 1.3 g/kg of albumin induced the EP depression to be 35.0 +/- 4.8 and 8.1 +/- 1.9 mV, respectively, and both prolonged the time to attain the minimum EP. However, there was no difference in the recovery time of the EP between the two groups. The results indicate that access to the site of furosemide action in the cochlea is dependent on the unbound fraction of furosemide and that the albumin-bound furosemide alleviates the EP depression induced by furosemide alone with the augmentation of diuresis.

Animals↗

PubMed2000

Effects of high-dose furosemide and small-volume hypertonic saline solution infusion in comparison with a high dose of furosemide as a bolus, in refractory congestive heart failure.

BACKGROUND: Diuretics, have been accepted as first-line treatment in refractory heart failure, but a lack of response is a frequent event. A randomised single blind study was performed to evaluate the effects of the combination of high-dose furosemide and small-volume hypertonic saline solution (HSS) infusion in the treatment of refractory NYHA class IV congestive heart failure (CHF). MATERIALS AND METHODS: Sixty patients (21 F/39 M) with refractory CHF (NYHA class IV) of different etiologies, unresponsive to high oral doses of furosemide, ACE-inhibitors, digitalis, and nitrates, aged 65-90 years, were enrolled. They had to have an ejection fraction (EF) <35%, serum creatinine <2 mg/dl, BUN </=60 mg/dl, a reduced urinary volume and a low natriuresis. The patients were randomised in two groups (single blind): group 1 (11 F/19 M) received an i.v. infusion of furosemide (500-1000 mg) plus HSS (150 ml of 1.4-4.6% NaCl) b.i.d. in 30 min. Group 2 (10 F/20 M) received an i.v. bolus of furosemide (500-1000 mg) b.i.d., without HSS, during a period lasting 6-12 days. Both groups received KCl (20-40 mEq.) i.v. to prevent hypokalemia. All patients underwent at entry a physical examination, measurement of body weight (BW), blood pressure (BP), heart rate (HR), evaluation of signs of CHF, and controls of serum Na, K, Cl, bicarbonate, albumin, uric acid, creatinine, urea and glycemia and daily during hospitalization, as well as the daily output of urine for, Na, K and Cl measurements. Chest X-ray, ECG and echocardiogram were obtained at entry during and at the discharge. During the treatment and after discharge the daily dietary Na intake was 120 mmol with a drink fluid intake of 1000 ml daily. An assessment of BW and 24-h urinary volume, serum and urinary laboratory parameters, until reaching a compensated state, were performed daily, when i.v. furosemide was replaced with oral administration (250-500 mg/day). After discharge, patients were followed as outpatients weekly for the first 3 months and subsequently once per month. RESULTS: The groups were similar for age, sex, EF, risk factors, treatment and etiology of CHF. All patients showed a clinical improvement. Six patients in both groups had hyponatremia (from 120 to 128 mEq./l) at entry. A significant increase in daily diuresis in both groups was observed (from 390+/-155 to 2100+/-626, and from 433+/-141 to 1650+/-537 ml/24 h, P<0.05). Natriuresis (from 49+/-15 to 198+/-28 mEq./24 h) was higher in group 1 vs. group 2 (from 53.83+/-12 to 129+/-39 mEq./24 h, P<0.05). Serum Na (from 135.9+/-6.8 to 142.2+/-3. 8 mEq./l, P<0.05) increased in the group 1 and decreased in the group 2 (from 134.7+/-7.9 to 130.1+/-4.3 mEq./l). Serum K was decreased (from 4.4+/-0.6 to 3.9+/-0.6, and 4.6+/-9 to 3.6+/-0.5 mEq. /l, P<0. 05) in both groups. BW was reduced (from 73.8+/-9.1 to 63. 8+/-8.8, and from 72.9+/-10.2 to 64.5+/-7.5 kg, P<0. 05) in both groups. Group 2 showed more patients in NYHA class III than group 1 (18 vs. 2 patients, P<0.05). Group 2 showed an increase of serum creatinine. Serum uric acid increased in both groups. BP values decreased, and HR was corrected to normal values in both groups. Group 2 showed a longer hospitalization time than group receiving HHS infusion (11.67+/-1.8 vs. 8.57+/-2.3 days, P<0.001). In the follow-up (6-12 months), none of the patients from group 1 were readmitted to the hospital and they maintained the NYHA class achieved at the discharge. Group 2 showed 12 patients readmitted to hospital and a higher class than at discharge. CONCLUSION: Our data suggest that the combination of furosemide with HSS is feasible and it appears that this combination produces an improvement of hemodynamic and clinical parameters, reduces the hospitalization time and maintains the obtained results over time in comparison with those receiving high-dose furosemide as bolus.

Aged↗

PubMed1988

Urinary excretion and diuretic action of furosemide in rats: increased response to the urinary excretion rate of furosemide in rats with acute renal failure.

A urinary excretion-response curve representing the urinary excretion rate of furosemide versus the urinary excretion rate of (Na+ + K+) was used to analyze furosemide action in rats with uranyl nitrate-induced acute renal failure (ARF) with and without dopamine coadministration. Urinary excretion of furosemide, but not its serum concentration, was the determinant for the diuretic action of furosemide. Increased diuretic response was observed in ARF rats, although the total diuretic response and urinary recovery of furosemide within 2 hr decreased. Dopamine enhanced furosemide-induced diuresis in ARF rats in terms of the total urine output and urinary electrolyte excretion, although the urinary excretion-response curves were not different. This enhancement by dopamine was found to be caused by the augmented urinary excretion of furosemide and the increased response to this drug in ARF rats. These findings suggest the contribution of decreased concentrating ability along the nephron and/or increased sensitivity of cells at the site of action to this drug.

Acute Kidney Injury↗

PubMed2001

Estimation of the probability for exceeding thresholds of urine specific gravity and plasma concentration of furosemide at various intervals after intravenous administration of furosemide in horses.

OBJECTIVE: To estimate the probability of concurrently exceeding thresholds for plasma concentration of furosemide and urine specific gravity after IV administration of furosemide in horses. ANIMALS: 12 mature healthy Thoroughbred (n = 6) or Quarter Horse (6) mares. PROCEDURE: Venous blood was collected from each horse prior to and 0.25, 0.5, 0.75, 1, 2, 3, 4, 4.5, 5, and 6 hours after IV administration of 250 mg (first experiment) or 500 mg (second experiment) of furosemide. Urine was collected hourly between 1 and 6 hours after administration of furosemide at both doses. Concentrations of furosemide were determined by use of an ELISA. Concentration of furosemide and urine specific gravity was modeled as a function of time, accounting for inter- and intrahorse variabilities. On the basis of pharmacokinetic and specific gravity data, the probability of exceeding a concentration of 100 ng of furosemide/ml as a function of time was determined, using a semiparametric smooth functional averaging method. A bootstrap approach was used to assess the inherent variation in this estimated probability. RESULTS: The estimated probability of exceeding the threshold of 100 ng of furosemide/ml and urine specific gravity < 1.012 was approximately 0% between 4.0 and 5.5 hours after IV administration of 250 mg of furosemide/horse, and ranged from 0 to 1% between 4 and 5.5 hours after IV administration of 500 mg of furosemide/horse. The probability of a horse being falsely identified as in violation of regulatory concentrations was inversely associated with time. CONCLUSIONS AND CLINICAL RELEVANCE: Coupling plasma furosemide concentration with urine specific gravity testing will greatly reduce the chance that some horses are misclassified as being in violation of regulatory concentrations.

Animals↗

PubMed1996

Effect of furosemide oral solution versus furosemide tablets on diuresis and electrolytes in patients with moderate congestive heart failure.

Oral furosemide solution was claimed to produce a greater diuretic response than furosemide tablets in patients with congestive heart failure. The aim of this study was to assess this observation and to further investigate the effects on the electrolyte balance. We compared the effects of oral furosemide in tablets versus oral furosemide solution on serum levels as well as on 4- and cumulative 24-hour urinary volume and sodium, potassium, calcium, magnesium and zinc excretions in 10 patients with moderate congestive heart failure due to ischemic heart disease. Oral furosemide (40-80 mg) was given at the usual once-daily dosage. No change in serum electrolyte levels has been found. All urinary parameters, except zinc, were significantly greater during the first 4 h following oral solution as compared with tablets (volume p < 0.001, sodium p < 0.001, potassium p < 0.05, calcium p < 0.003, magnesium p < 0.05). However, after 24 h, significant differences were found in urinary volume (p < 0.03) and sodium excretion (p < 0.004) only. We conclude that: (1) oral furosemide solution provides a more potent 24-hour diuretic and natriuretic effect than an identical dosage in tablet form, without entailing greater cumulative urinary losses of potassium, calcium, magnesium, and zinc; (2) following the first 4 h of furosemide solution, brisk diuresis, kaliuresis, and magnesiuria are produced, and (3) despite the urinary losses, serum electrolytes remained within normal limits at 4 and 24 h.

Aged↗

PubMed1984

Efficacy of metolazone and furosemide in children with furosemide-resistant edema.

The effect of a combination of metolazone (0.2 to 0.4 mg/kg/d) and furosemide (2 to 4 mg/kg/d) in achieving a natriuresis and diuresis was measured in 14 children during 22 episodes of edema resistant to furosemide alone. Urinary volume increased from 24 +/- 14 mL/kg/d for patients receiving furosemide to 51 mL/kg/d with combined diuretic therapy (P less than .01), and sodium excretion increased from 34 +/- 5 mEq/d to 155 +/- 176 mEq/d (P less than .01). Two children with severe hypoalbuminemia (serum albumin level less than 1.5 g/dL) and normal renal function, and five children with chronic renal insufficiency (71%) did not respond to combined diuretic therapy. The combination of furosemide and metolazone offers a useful and effective oral therapy in most children with edema resistant to furosemide. Children with chronic renal insufficiency and furosemide-resistant edema did not respond to combination diuretic therapy.

Adolescent↗

PubMed1986

Effects of furosemide and slow-release furosemide on thoracic fluid volumes.

Transthoracic electrical impedance (TEI) was used to assess the relative effectiveness of a 60 mg sustained-release furosemide preparation (FR) and a 40 mg standard furosemide tablet (F), in reducing the fluid content in the thoracic cavity. A double-blind crossover study was performed, in which 12 men with a history of one or more myocardial infarctions and mild left heart failure treated with 40 mg furosemide once daily participated. The trial, lasting 28 days, was divided into two 14-day periods. Each participant received one active drug and one placebo preparation daily, the same regimen being maintained for 14 days, when the active substances were switched. TEI, body weight, serum potassium, sodium, creatinine, and urate were measured immediately prior to the start of the study, after 14 days, and at the end of the study. TEI was measured at frequencies of 1 and 100 kHz with a constant current of 100 microA, during a period of one hour following an intravenous injection of 40 mg furosemide, when the urine volumes were measured also. TEI and urine production after the furosemide injections were similar irrespective of the drug preparation. No evidence of treatment period interaction was seen. No significant differences were demonstrated in body weight and blood chemistry during the trial. These results suggest clinical equipotency of the two preparations in mild left heart failure.

Aged↗

PubMed1998

Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema.

BACKGROUND: Nitrates and furosemide, commonly administered in the treatment of pulmonary oedema, have not been compared in a prospective clinical trial. We compared the efficacy and safety of these drugs in a randomised trial of patients with severe pulmonary oedema and oxygen saturation below 90%. METHODS: Patients presenting to mobile emergency units with signs of congestive heart failure were treated with oxygen 10 L/min, intravenous furosemide 40 mg, and morphine 3 mg bolus. 110 patients were randomly assigned either to group A, who received isosorbide dinitrate (3 mg bolus administered intravenously every 5 min; n=56) or to group B, who received furosemide (80 mg bolus administered intravenously every 15 min, as well as isosorbide dinitrate 1 mg/h, increased every 10 min by 1 mg/h; n=54). Six patients were withdrawn on the basis of chest radiography results. Treatment was continued until oxygen saturation was above 96% or mean arterial blood pressure had decreased by 30% or to below 90 mm Hg. The main endpoints were death, need for mechanical ventilation, and myocardial infarction. The analyses were by intention to treat. FINDINGS: Mechanical ventilation was required in seven (13%) of 52 group-A patients and 21 (40%) of 52 group-B patients (p=0.0041). Myocardial infarction occurred in nine (17%) and 19 (37%) patients, respectively (p=0.047). One patient in group A and three in group B died (p=0.61). One or more of these endpoints occurred in 13 (25%) and 24 (46%) patients, respectively (p=0.041). INTERPRETATION: High-dose isosorbide dinitrate, given as repeated intravenous boluses after low-dose intravenous furosemide, is safe and effective in controlling severe pulmonary oedema. This treatment regimen is more effective than high-dose furosemide with low-dose isosorbide nitrate in terms of need for mechanical ventilation and frequency of myocardial infarction.

Acute Disease↗

PubMed2003

Effects of high-dose furosemide and small-volume hypertonic saline solution infusion in comparison with a high dose of furosemide as bolus in refractory congestive heart failure: long-term effects.

BACKGROUND: Diuretics have been accepted as first-line treatment in refractory congestive heart failure (CHF), but a lack of response to them is a frequent event. A randomized, single-blind study was performed to evaluate the effects of the combination of high-dose furosemide and small-volume hypertonic saline solution (HSS) infusion in the treatment of refractory New York Heart Association (NYHA) class IV CHF and a normosodic diet during follow-up. Materials and Methods One hundred seven patients (39 women and 68 men, age range 65-90 years) with refractory CHF (NYHA class IV) of different etiologies, who were unresponsive to high oral doses of furosemide, angiotensin-converting enzyme inhibitors, digitalis, and nitrates, were enrolled. Inclusion criteria included an ejection fraction (EF) <35%, serum creatinine level <2 mg/dL, blood urea nitrogen level < or =60 mg/dL, reduced urinary volume, and low natriuresis. The patients were randomized in 2 groups (single-blind). Patients in group 1 (20 women and 33 men) received an intravenous (IV) infusion of furosemide (500-1000 mg) plus HSS (150 mL of 1.4%-4.6% NACl) twice a day in 30 minutes. Patients in group 2 (19 women and 35 men) received an IV bolus of furosemide (500-1000 mg) twice a day, without HSS, during a period lasting 6 to 12 days. Both groups received IV KCl (20-40 mEq) to prevent hypokalemia. At study entry, all patients underwent a physical examination and measurement of body weight (BW), blood pressure (BP), and heart rate (HR), an evaluation of signs of CHF, and measurement of control levels of serum Na, K, Cl, bicarbonate, albumin, uric acid, creatinine, urea, and glycemia daily during hospitalization, and measurements of the daily output of urine for Na, K, and Cl. A chest radiograph, electrocardiogram, and echocardiogram were obtained at study entry, during hospitalization, and at the time of discharge from the hospital. During the treatment and after discharge, the daily dietary Na intake was 120 mmol in group 1 versus 80 mmol in group 2, with a fluid intake of 1000 mL daily in both groups. An assessment of BW and 24-hour urinary volume, serum, and urinary laboratory parameters were performed daily until patients reached a compensated state, when IV furosemide was replaced with oral administration (250-500 mg/d). After discharge from the hospital, patients were observed as outpatients weekly for the first 3 months and, subsequently, once a month. RESULTS: The groups were similar in age, sex, EF, risk factors, treatment, and etiology of CHF. All patients showed a clinical improvement. Ten patients in both groups had hyponatremia at entry. A significant increase in daily diuresis and natriuresis was observed in both groups, but it was more significant in the group receiving HSS (P <.05). The serum Na level increased in group 1 and decreased in group 2 (P <.05). The serum K level was decreased in both groups (P <.05). BW was reduced in both groups (P <.05). Group 2 had an increase in serum creatinine level. Serum uric acid levels increased in both groups. BP values decreased and HR was corrected to normal values in both groups. In the follow-up period (31 +/- 14 months), 25 patients from group 1 were readmitted to the hospital for heart failure. In group 2, 43 patients were readmitted to the hospital at a higher class than at discharge. Twenty-four patients in group 1 died during follow-up, versus 47 patients in group 2 (P <.001). CONCLUSION: This treatment is effective and well tolerated, improves the quality of life through the relief of signs and symptoms of congestion, and may delay more aggressive treatments. The effects were also beneficial in a long period for mortality reduction (55% vs 13% survival rate) and for clinical improvement.

Administration, Oral↗

PubMedDate not supplied

The pharmacology of furosemide in the horse. V. Pharmacokinetics and blood levels of furosemide after intravenous administration.

Studies were undertaken to determine blood levels of furosemide in horses after 0.5- and 1.0-mg/kg doses administered iv. Analyses indicated that the pharmacokinetic parameters were dose independent and best described by a three-compartment open model. The alpha-, beta-, and gamma-phase half-lives of 5.6, 22.3, and 158.5 min, respectively, were observed after the 0.5-mg/kg dose. Similarly, the respective half-lives after the 1.0-mg/kg dose were 5.8, 24.1, and 177.2 min. After a 0.5-mg/kg dose of furosemide, population frequency distributions were evaluated at 1 hr and 4 hr post-drug administration. At 1 hr after dosing, the blood levels of furosemide in 30 horses were normally distributed. The mean plasma level was 97.9 ng/ml with a range of 41.9 ng/ml to 155.8 ng/ml and a SD of 25.0 ng/ml. Analyses of blood levels of furosemide in 47 horses at 4 hr after drug administration indicated that the population distribution was better fit by a normal curve after log transformation of the values. The mean plasma level at 4 hr post-dosing was 9.6 ng/ml with a range of 4.0 ng/ml to 19.4 ng/ml and a SD of 3.1 ng/ml. Based on this population distribution of the plasma levels, the probability of finding furosemide plasma concentrations above 24.6 ng/ml at 4 hr after anti-epistaxis dose was estimated at less than 1 in 1000.

Animals↗

PubMed1980

Response of renin, aldosterone and antidiuretic hormone to furosemide and furosemide-triamterene combination.

Plasma renin activity (PRA), antidiuretic hormone (ADH), urinary aldosterone excretion (U-Aldo) and electrolyte excretions were studied in a randomized study after furosemide (80 mg) (F), furosemide + triamterence (80 + 100 mg) (F + T), and after placebo were administered to seven healthy volunteers. F + T preparation showed a slower absorption of furosemide, a slower natriuresis and a slower excretion of potassium as compared to F-präparation. After application of the diuretics, PRA reached the maximal level in four hours, three times higher than the control level after F and four times higher after F + T. At 24 hrs after drug intake PRA did not differe from the control level. No significant difference could be found between F and F + T. U-Aldo of 24 hrs increased 1.9-fold after F and 2.2-fold after F + T, as compared with placebo. Between the individual natriuretic and hormonal responses no correlation could be found. After F + T, U-Aldo and U-K showed a positive correlation (P < 0.05). ADH did not change after diuretics from the pretreatment fasting level. The results show a fast but transient response of the renin-aldosterone system after furosemide and the furosemide-triamterene combination which could not be correlated with the natriuretic effects. The result differs from that found earlier with hydrochlorothiazide.

Adult↗

PubMed1990

Comparison of the diuretic effect and absorption of a single dose of furosemide and free and the fixed combinations of furosemide and triamterene in healthy male adults.

The absorption and diuretic effect of furosemide 40 mg alone (F), and of the free (F + T) and the fixed (FT) combinations of furosemide 40 mg and triamterene 50 mg have been compared in 12 healthy young men. A slight reduction in the area under the concentration-time curve (AUC) of plasma furosemide was found for the fixed combination (AUC480) F2.58 micrograms.h.ml-1; F + T 2.46 micrograms.h.ml-1; FT 1.97 micrograms.h.ml-1. There was a significant reduction in the AUC480 of plasma triamterene (F + T 204.9 micrograms.h.l-1; FT 130.2 micrograms.h.l-1). Sodium excretion after F + T and FT was more pronounced than after F (F + T 302 mmol; FT 311 mmol; F259 mmol). When compared to F alone, there was a reduction in the 24-hour potassium excretion after F + T as well as after FT (F 121 mmol; F + T 104 mmol; FT 107 mmol). It is concluded that the absorption of triamterene was significantly reduced after ingestion of the fixed combination tablet. However, in healthy male adults this had no influence on its natriuretic and potassium-sparing effect as compared to the free combination.

Absorption↗

PubMed2005

Changes in brain natriuretic peptide levels and bioelectrical impedance measurements after treatment with high-dose furosemide and hypertonic saline solution versus high-dose furosemide alone in refractory congestive heart failure: a double-blind study.

OBJECTIVES: The aim of this study was to evaluate the effect of a new treatment for refractory congestive heart failure (CHF) on brain natriuretic peptide (BNP) plasma levels and hydration station. BACKGROUND: The study was aimed at evaluating the effects of the combination of high-dose furosemide and small-volume hypertonic saline solution (HSS) in refractory CHF patients. METHODS: A total of 94 patients (34 women/60 men) with refractory CHF (age 55 to 80 years) were enrolled. They had to have an ejection fraction <35%, serum creatinine <2 mg/dl, blood urea nitrogen <60 mg/dl, a reduced urinary volume, and a low natriuresis (<500 ml/24 h and <60 mEq/24 h, respectively). Patients were divided (double-blind) into two groups: group 1 (18 women/30 men) received an intravenous furosemide (500 to 1,000 mg) plus HSS twice a day in 30 min. Group 2 (16 women/30 men) received an intravenous bolus of furosemide (500 to 1,000 mg/twice a day) alone, for four to six days. At entry, body weight, blood pressure, heart rate, and laboratory parameters were checked during hospitalization; BNP levels were measured on admission, 6 and 30 days after discharge, while on admission and 6 days after, impedance plethysmography was performed. The HSS group received 120 mmol of Na intake versus 80 mmol in non-HSS group. Fluid intake of 1,000 was given to both groups. RESULTS: The groups were similar for clinical characteristics. A significant increase in daily diuresis and natriuresis was observed in HSS group, p < 0.05. The BNP values showed significant intragroup and intergroup differences, 6 and 30 days after treatment. The patients from the HSS group reached a better hydration state than the non-HSS group after six days. In addition, the HSS group showed a significant reduction in hospitalization time and readmission rate. CONCLUSIONS: Our data show that the HSS group reached dry weight more rapidly, a significantly faster reduction in BNP levels, shorter hospitalization stay, and lower incidence in readmissions in the 30-day study period.

Aged↗

PubMed1975

Application of the carbonic anhydrase inhibitory effect of furosemide to the study of furosemide release from two of its diuretic derivatives.

Bovine carbonic anhydrase B (CA) inhibitory effect of furosemide was established in two pH values at 26 degress. FFBu [N-furfuryl-4-chloro-5-(butoxymethylsulfamoyl)anthranilic acid] and FFMe [N-furfuryl-4-chloro-5-(methoxy-methylsulfamoyl)anthranilic acid], two of its alkoxymethyl derivatives, did not exert any CA inhibitory effect at those conditions but were found to inhibit the CA activity after their hydrolysis, which yielded the furosemide molecule. The CA inhibitory effect of furosemide was utilized for determining the kinetic rate constants for the hydrolysis of FFBu and FFMe at various pH and temperature levels. The hydrolysis rate constants of FFBu and FFMe were pH-independent in the pH range tested, and the temperature dependence for FFBu yielded an activation energy of 18 kcal/mol. It is pointed out that the hydrolysis rates of FFBu may be important for the explanation of its possible delayed diuretic effect.

Carbonic Anhydrase Inhibitors↗