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PubMedDate not supplied

Comparative bioavailability of furosemide from solution and 40 mg tablets with different dissolution characteristics following oral administration in normal men.

Furosemide tablets, with markedly different dissolution characteristics, and solution were orally administered to 21 healthy adult males to determine the effect of in vitro dissolution rate on in vivo bioavailability profiles. Furosemide 40 mg was given as Tablet A (fast dissolution characteristics), Tablet B (slow dissolution characteristics), and an aqueous solution. Both batches of tablets had identical formulae and were produced by a common process. The dissolution rate of the slower Tablet B was probably retarded by extension of the wet granulation time. Blood was collected for 12 h postdose and urine for 24 h. Peak plasma furosemide concentrations after the solution were significantly greater than after the tablets; there was no significant difference between the tablets. The time to peak occurred significantly earlier with the solution, with no significant difference between the tablets. Relative bioavailabilities of Tablet A and B were 89 per cent and 101 per cent, respectively, as determined by AUC, and 79 per cent and 84 per cent, respectively, as determined by urine recovery. These differences are not statistically significant. These results indicate that dissolution rate profiles of furosemide tablets may not be predictive of in vivo bioavailability.

Administration, Oral↗
PubMed1976

Furosemide and bumetanide: a study of responses in normal English and German subjects.

Diuretic responses to oral administration of 1 mg bumetanide and 40 mg furosemide were determined in double-blind, crossover balanced trials in 10 normal English subjects and 6 normal German subjects. In each experiment the 0- to 8-hr urine volume and sodium excretion were significantly higher after bumetanide, potassium excretion did not differ, and the Na/K ratio, although higher after bumetanide, was not significantly different by analysis of variance. In German subjects the diuretic and natriuretic responses to both drugs were greater and the potassium excretion less than in English subjects. In the English, the pretreatment 24-hr urinary Na/K ratio correlated with the urinary Na/K ratio response to both drugs and with the potassium excretion after furosemide. The mean plasma uric acid before treatment correlated with the Na/K ratio and potassium excretion after furosemide. Aldosterone excretion did not correlate with response to either diuretic. The mean pretreatment 24-hr log10 Na/K ratio in the two treatment periods of the English and German subjects correlated with the mean sodium excretion, potassium excretion, and log10 Na/K after the two diuretics, thus providing a partial explanation for intersubject and interstudy variation. Pretreatment log10 Na/K could also explain intrasubject variation, justifying its use as a covariate in covariance analysis. This demonstrated that at this dose ratio the urinary log10 Na/K ratio response to bumetanide was significantly higher than that to furosemide.

Aldosterone↗
PubMed1978

Placental transfer of furosemide.

After oral administration of furosemide to 18 pregnant women on the day of delivery, substantial concentrations of the drug were detected in umbilical cord vein plasma as well as in amniotic fluid. The ratio between the furosemide concentrations in maternal vein plasma and in umbilical cord plasma increased with time and approximated unity at 8 to 10 hr after administration of the drug. The plasma half-life of furosemide appeared to be longer in the mothers than in nonpregnant healthy volunteers. In one patient the plasma level of furosemide was constant during 5 hr of observation.

Amniotic Fluid↗
PubMed1979

Azosemide, a "loop" diuretic, and furosemide.

Azosemide is a new monosulfamyl diuretic which inhibits solute transport throughout the thick ascending limb of the loop of Henle. This study compared equal amounts of azosemide and furosemide (20, 40, and 80 mg) in normal subjects. No differences occurred at any dose in volume, sodium, or chloride excretion when analyzed as cumulative excretion at 4, 8, or 12 hr. Azosemide 40 mg caused less potassium excretion than 40 mg of furosemide but there was no significant difference in the sodium/potassium excretion ratio. Analysis of the time course of effect showed that compared to furosemide azosemide tended to have a slower onset of effect. Differences in site of action studies between azosemide and furosemide did not manifest as differences in urinary or electrolyte excretion in our normal subjects.

Adult↗
PubMedDate not supplied

Effects of a new loop diuretic (muzolimine) in cirrhosis with ascites: comparison with furosemide.

Muzolimine is a loop diuretic with both the dose-dependent increasing effectiveness of loop diuretics and the long-lasting effect of thiazides. This is a potential advantage in the treatment of ascites in advanced cirrhosis since these patients have a low tolerance to sudden reductions of blood volume. Equivalent single, oral doses of furosemide (40 mg) and muzolimine (30 mg) were given to 10 cirrhotic patients with ascites and reduced renal perfusion (glomerular filtration rate = 30 to 75 ml per min). The study was preceded by 4 days of equilibration (dietary sodium 40 mmoles per day), and the drugs were alternated via a single-blind, cross-over protocol after a wash-out period of 3 days. Renal function was monitored under basal conditions and after diuretic administration through 4-hr clearance periods for 24 hr. The renin-aldosterone axis was evaluated before diuretic administration and after 8 and 24 hr. Muzolimine led to a 12-hr cumulative diuresis [AUC0-12 = 2.52 +/- 0.42 (S.E.) ml per min] and natriuresis (5.14 +/- 1.05 mmoles per hr), which were comparable to those of furosemide (2.85 +/- 0.29 ml per min and 6.75 +/- 1.63 mmoles per hr). Its effect, however, was distributed over a longer period (8 hr) than furosemide (4 hr). Muzolimine activity mainly differed from furosemide because of: significantly lower 12-hr potassium excretion (AUC0-12 = 0.28 +/- 0.82 vs. 2.69 +/- 0.46 mmoles per hr; p less than 0.005); greater sodium/chloride excretion ratio (0.45 +/- 0.08 vs. 0.26 +/- 0.06; p less than 0.025), and absence of rebound phenomena.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMedDate not supplied

The effect of furosemide and bumetanide on warfarin metabolism and anticoagulant response.

In a study of 11 normal subjects who received either furosemide or bumetanide, response to warfarin was unaffected by either diuretic. The mean prothrombin times after a single oral dose of 50 mg warfarin were 18.8 +/- 0.7 sec before and 19.6 +/- 1.7 sec during furosemide administration, and 18.3 +/- 1.4 sec before and 19.7 +/- 1.3 sec during bumetanide administration. Mean plasma warfarin half-lives were 43.2 +/- 2.8 hr before and 37.8 +/- 1.7 hr during furosemide treatment and 39.9 +/- 9.5 hr before and 37.4 +/- 2.4 hr during bumetanide treatment. Hypoprothrombinemic responses, plasma warfarin concentrations, and warfarin half-lives were not significantly influenced by treatment with either diuretic. Both loop diuretics furosemide and bumetanide can be safely administered during warfarin anticoagulant therapy without risk of clinically significant interaction.

Adolescent↗
PubMed1980

The role of furosemide alone and in combination with digoxin in the relief of symptoms of congestive heart failure.

Clinical and cardiovascular responses to drug therapy with furosemide were compared with those to furosemide plus digoxin in 15 heart patients with sinus rhythm admitted to the hospital for the management of congestive heart failure. Except for two patients in the group treated with furosemide alone, who required the addition of intravenous furosemide for more complete relief of symptoms, the responses to the two therapeutic regimens were not significantly different. One patient in the digoxin-treated group developed atrial fibrillation with frequent ventricular premature beats and transient runs of bigeminal rhythm typical of digitalis toxicity, which disappeared as the dose of digoxin was lowered. Side effects were otherwise considered to be minor and similar in the two groups. The results support the view that the indications for digoxin as a positive inotropic agent in patients with congestive heart failure need to be reevaluated.

Adult↗
PubMedDate not supplied

Electrolyte excretion patterns. Intravenous and oral doses of bumetanide compared to furosemide.

The response to bumetanide and furosemide administered orally and intravenously was compared in normal subjects. Doses of bumetanide were 0.5 and 1 mg intravenously and 0.5, 1 and 2 mg orally. Doses of furosemide were 20 and 40 mg intravenously and 20, 40, and 80 mg orally. After intravenous doses of both drugs, peak natriuresis occurred during the first collection period of 30 minutes and the response returned to baseline by 3.5 hours. After oral dosing, peak effect occurred at 75 minutes and returned to baseline within 4 hours. Cumulative response was assessed for volume, sodium, potassium, and chloride excretion. The response did not differ substantially between drugs. On a milligram basis, bumetanide was approximately 50 times as potent as furosemide. For both drugs, the intravenous dose was approximately three times as potent as the oral preparation. The time course of response shows that the curves are virtually superimposable. The diuretic effect was short-lived for both diuretics. The urine volume and sodium and chloride excretion were parallel. The sodium/potassium ratio was calculated as follows: for every 200 mEq sodium excreted in 4 hours, bumetanide caused about 35 mEq and furosemide caused about 50 mEq potassium to be eliminated. Even if statistically significant, this difference does not appear to be clinically remarkable. If bumetanide offers therapeutic advantages in this regard, studies in patients with various disease states would have to be performed.

Administration, Oral↗
PubMedDate not supplied

Comparative ototoxicity of bumetanide and furosemide when used in combination with kanamycin.

The ototoxicity of bumetanide and furosemide was compared in Topeka strain guinea pigs pretreated with kanamycin. The animals, anesthetized with pentobarbital, received a single dose of 400 mg/kg kanamycin subcutaneously and the diuretics via indwelling catheter in the jugular vein 2 hours later. Ototoxic drug effects were determined by measuring the electrophysiological responses of the cochlea to sound stimuli and by determining the presence or absence of cochlear sensory hair cells from the organ of Corti. Both bumetanide and furosemide produced permanent alteration of cochlear activity in the kanamycin-pretreated animals. The ototoxic effect of bumetanide is five times that of furosemide on a milligram-for-milligram basis. The ototoxic potential of bumetanide is one eighth that of furosemide when the doses are adjusted for diuretic potency difference between the two diuretics.

Animals↗
PubMedDate not supplied

Clinical trial of bumetanide versus furosemide in patients with congestive heart failure.

A clinical trial was conducted in open, randomized, parallel fashion to determine the effectiveness and safety of bumetanide compared with those of furosemide in 42 outpatients with edema due to congestive heart failure. All patients were free from any significant hepatic or renal disease. The duration of the study was six months, except for 12 patients who were continued under treatment with bumetanide for an additional six months. Changes in body weight, edema, abdominal girth, hepatomegaly and other signs of congestive heart failure were evaluated. No statistically significant differences between bumetanide and furosemide were noted in these clinical parameters. Blood pressure was decreased in both groups, more consistently with furosemide, but without statistical significance. Laboratory tests revealed only minor changes in serum sodium, potassium, chloride, and uric acid in both groups throughout the treatment period, with the exception of chloride in the bumetanide group at 8 and 16 weeks. The patients who received extended treatment maintained a relatively stable state. No clinical adverse reactions were considered to be related to either drug. Both diuretics proved equally effective in reducing edema. The effective dose ratio of bumetanide:furosemide was 1:25.

Adult↗
PubMedDate not supplied

A comparison of bumetanide and furosemide in the treatment of ascites. Cooperative study.

In a cooperative study by clinicians in three medical facilities, bumetanide was compared with furosemide in patients presenting with ascites, a complication of chronic liver disease. In an open, parallel, randomized trial, 43 patients received bumetanide and 16 patients received furosemide. They were treated for from one to 28 weeks. Weight loss and decrease in abdominal girth following diuretic action occurred in both groups but was statistically significant only in the bumetanide treated patients. Because of the small number of patients on furosemide, valid statistical analysis could not be obtained. No evidence of hepatic encephalopathy developed during this study, and only one patient on furosemide was discontinued as a result of severe electrolyte imbalance. Differences in changes of electrolytes and uric acid ere not statistically significant in the two groups. The majority of drug-related abnormalities were the result of the pharmacologic activity of the diuretic.

Adult↗
PubMed1986

Effects of low-dose aspirin on responses to furosemide.

We assessed the effects of low-dose aspirin (0.5 and 15 mg/kg/d) on renal prostaglandin synthesis and action in healthy volunteers using intravenous furosemide as a stimulus. Inhibition of platelet cyclo-oxygenase was assessed by changes in serum thromboxane B2 (TXB2) level. After one week of treatment, ten healthy subjects did not show any change in weight, blood pressure, or diuretic and natriuretic responses to furosemide with either dose of aspirin. Serum TXB2 level was reduced to 3% of control by aspirin 0.5 mg/kg/d and to 0.1% by the higher dose. In contrast, urine excretion of TXB2 was only reduced to 68% and 51% of the placebo value, whereas 6-keto-prostaglandin F1 alpha (6kPGF1 alpha) excretion was not decreased by either dose. Furosemide produced a transient increase in excretion rates of TXB2 and 6kPGF1 alpha that was of lesser duration than the diuretic response. These transient increases were slightly reduced by aspirin. Baseline plasma renin activity was not affected by either dose of aspirin. The brisk increment in plasma renin activity seen ten minutes after furosemide, as well as later values (30 and 240 min) were not changed by aspirin. We conclude that chronic low-dose aspirin can profoundly affect platelet PG production without affecting stimulated renal PGI2 production or plasma renin activity. There is a modest reduction in urine TXB2 excretion that is consistent with a primarily renal source of this metabolite.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

No evidence of a direct venodilatory effect of furosemide in healthy human subjects.

The present study was undertaken to examine whether furosemide, a loop diuretic, has a direct venodilatory effect in healthy male subjects. Furosemide, or amrinone, an inotropic agent with a vasodilatory action, was infused into a dorsal hand vein that had been preconstricted by phenylephrine. The diameter of the vein was measured by a linear variable differential transformer. Venodilation was observed during the infusion of amrinone, but such a response was not detected with furosemide. These findings do not support the hypothesis that furosemide has a direct venodilatory effect in healthy human subjects.

Adult↗
PubMed1998

A randomized, placebo-controlled study of loop diuretics in patients with essential hypertension: the bumetanide and furosemide on lipid profile (BUFUL) clinical study report.

This study was conducted to determine whether loop diuretics are more effective than placebo in reducing blood pressure without raising serum lipid levels, and whether bumetanide is more effective than furosemide in this respect. In a double-blind, 24-week placebo-controlled crossover study, 27 patients with essential hypertension were treated in four periods of 6 weeks each, including placebo twice, furosemide 40 mg daily, and bumetanide 1 mg daily. Several metabolic parameters, including serum lipid levels, and blood pressure were assessed. Overall levels of total cholesterol, triglycerides, and low-density lipoprotein (LDL) cholesterol were 5%, 12.4%, and 4.8% higher, respectively, during loop diuretic therapy than during placebo treatment. Overall systolic and diastolic blood pressure measurements were 12 mmHg and 4 mmHg lower, respectively, during loop diuretic therapy than during placebo treatment. Any added effect of bumetanide on serum lipid levels and blood pressure compared with furosemide, however, could not be confirmed. Our results indicate that the loop diuretics bumetanide and furosemide are effective in reducing blood pressure, and influence serum lipid levels markedly less than do thiazide diuretics or chlorthalidone. In addition, these results indicate that differences in blood pressure reduction and serum lipid levels between the two compounds were small and nonsignificant.

Adult↗
PubMed2002

Contributions of saturable active secretion, passive transcellular, and paracellular diffusion to the overall transport of furosemide across adenocarcinoma (Caco-2) cells.

Furosemide permeation across Caco-2 cells was investigated to determine if previously reported directional differences in transport rates are due to a saturable, energy dependent process. In addition, studies were carried out to determine the route of permeation for this drug. By comparing apical (A) to basolateral (B) and B to A directional transport across Caco-2 cells, a saturable, nonlinear component to furosemide transport was observed. Transport in the secretory direction was fit to yield the following apparent parameters K(m) = 63 +/- 28 microM, V(max) = 436 +/- 137 pmol/cm(2)h, and P(app) = 3.7 +/- 0.9 x 10(-7) cm/s. Evidence of energy dependence was demonstrated using both metabolic inhibition, and transport against a diffusion gradient methods. Disruption of tight junctions by use of the calcium chelator, EGTA, caused a significant increase in furosemide transport (twofold and 12-fold increases in B to A and A to B, respectively) indicating the importance of the paracellular route. We conclude that furosemide secretion from Caco-2 cells is the result of saturable active transport and passive diffusion that has a significant paracellular component.

Biological Transport, Active↗
PubMed1980

Preliminary evaluation of furosemide-probenecid interaction in humans.

The pharmacokinetics and pharmacodynamics of intravenous furosemide, 40 mg, were studied in four healthy male subjects in a crossover fashion with and without probenecid pretreatment. In each study, 16 plasma and 10 urine samples were collected over 24 hr. Fluid and electrolyte urinary losses were replaced orally throughout the study. Unchanged furosemide and probenecid were measured using high-pressure liquid chromatography; urinary sodium was measured by flame photometry. Although probenecid caused marked changes in the pharmacokinetic parameters of furosemide (increased area under the curve, decreased plasma and renal clearance, increased half-life, and decreased fraction excreted unchanged in the urine), there was no significant difference in its gross 8-hr natriuretic and diuretic effect. However, analysis of the time course of natriuresis showed a pattern similar to that of the urinary furosemide excretion rate, whereas the plasma concentration was poorly correlated over the entire dose-response curve.

Adult↗
PubMed1982

Disposition and absolute bioavailability of furosemide in healthy males.

Furosemide (40 mg) was administered to 18 healthy adult males as an intravenous dose, an oral solution, and in tablet form. The pharmacokinetics of intravenous furosemide were studied, determining a total body clearance rate of 117.6 +/- 41.3 ml/min and a harmonic mean half-life of 78 min. The mean absolute bioavailability determined by ratio of areas under the plasma-time curves was 64 and 71% for the solution and tablet, respectively. The mean absolute bioavailability determined by the ratio of urinary cumulative excretion data was 61 and 66% for the solution and tablet, respectively. The absolute bioavailability of furosemide determined with plasma and urine data were not significantly different. Thus, urine data alone may be used to establish bioavailability of furosemide. Inspection of plasma-time curves revealed secondary maxima in several subjects, suggesting enterohepatic cycling.

Administration, Oral↗
PubMed1991

Multiple linear regression modeling of furosemide renal clearance and urinary excretion rate.

Multiple linear regression techniques were utilized to determine models for the renal clearance and urinary excretion rate of furosemide. Models for the renal clearance were formulated based on data collected from the literature. The best model predicted that the weight-normalized renal clearance was a function of the weight-normalized creatinine clearance, with coefficient values dependent on the presence or absence of heart, liver, and/or kidney failure. The predictive performance of this model was evaluated using a separate verification data set, and, prospectively, for a group of cardiac patients. The urinary excretion rate of furosemide is the primary determinate of response. Models for the furosemide excretion rate were formulated from data collected prospectively from a group of patients with cardiac disease. The best model predicted that the dose-normalized morning urinary excretion rate was a function of the blood urea nitrogen concentration (BUN), with modifications for the presence of liver failure and/or decompensated heart failure. The oral dosage required to produce a clinically optimal furosemide excretion rate in cardiac patients without liver disease was dose (mg) = 42.1/(0.925-0.0151 BUN).

Aged↗