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PubMed1988

Effects of the diuretic furosemide on the sensitivity of glycolysis and glycogen synthesis to insulin in the soleus muscle of the rat.

The diuretic furosemide (0.5 mmol/l) impaired glucose uptake in the soleus muscle of the rat by decreasing the sensitivity of glycolysis to insulin. In addition, at higher concentrations (1.0 mmol/l) the drug inhibited the basal rate of glycolysis. It did not, however, inhibit the rate of glycogen synthesis except at a concentration of 6.0 mmol/l. Since furosemide has some structural similarities to adenosine, the above effects on insulin sensitivity may be due to its ability to act as an adenosine receptor agonist in muscle. These effects of furosemide in skeletal muscle may contribute to the glucose intolerance following therapy with this and similar agents in man.

Animals↗

PubMed1987

Absence of interaction between furosemide and mitomycin C.

The possible interaction between furosemide and mitomycin C (MMC) was studied in five patients. The pharmacokinetics of MMC were studied using an HPLC assay. Furosemide was administered prior to, or 120 min after MMC. Furosemide did not change the pharmacokinetics of MMC, nor did it change the amount of MMC excreted in the urine. There appears to be no interaction between the two drugs.

Adult↗

PubMed1985

The effect of furosemide on glucose oxidation of the cochlea and other tissues.

We tested the hypothesis that furosemide interferes with energy generation in the cochlea, and determined its effect on CO2 formation from glucose and glyceroaldehyde-3-phosphate dehydrogenase (GAPDH) activity by examining biochemical and histochemical changes in the cochlea, the kidney, and the liver. We found that furosemide suppressed CO2 formation in vitro at relatively low concentrations in all tissues examined. GAPDH was inhibited as soon as 2 min after its administration (80 mg/kg, i.v.). Recovery of this enzyme activity was most rapid in the liver. We concluded that furosemide does interfere with energy generation in the cochlea, kidney, and liver as a result of its inhibition of GAPDH.

Animals↗

PubMed1985

Attenuation of cisplatinum-induced nephrotoxicity in the rat by high salt diet, furosemide and acetazolamide.

The influence of variations in sodium chloride diet, furosemide and acetazolamide on nephrotoxicity induced by cisplatinum have been investigated in the rat by measuring serum creatinine concentrations 5 days after cisplatinum (5 mg/kg, ip) administration. Sodium chloride depletion enhanced, while sodium chloride loading minimized changes in renal function. Increases in urine flow rate following a dextrose water load failed to alter the nephrotoxic response. Both furosemide and acetazolamide, given 30 min before cisplatinum, attenuated the nephrotoxic response. In contrast, neither sodium chloride loading, furosemide, nor acetazolamide influenced the change in renal function when given 30 min after cisplatinum. These observations indicate that renal damage due to cisplatinum can be modified by alterations in dietary salt and by diuretics and that the extent of ultimate renal damage is dependent on factors occurring immediately after cisplatinum administration.

Acetazolamide↗

PubMed1985

Multicentre comparison between slow-release furosemide and bendroflumethiazide in congestive heart failure.

The effects of slow-release furosemide and bendroflumethiazide in the ambulatory treatment of mild to moderate congestive heart failure were compared in a controlled multicentre study using a randomized, double-blind procedure. In the first trial, slow-release furosemide 60 mg daily was compared with 2.5 mg bendroflumethiazide; in the second trial the daily doses were 30 mg and 2.5 mg, respectively. There were 47 patients in Trial I and 39 in Trial II. The randomised allocation to the treatment regimen was made after a four-week period on bendroflumethiazide 2.5 mg daily, and treatment was continued for 12 weeks. Clinical and laboratory data were recorded before, during and at the end of the trial. Adverse effects were few and minor in both medication groups, and there were no significant intergroup differences. It was concluded slow-release furosemide 30 mg or 60 mg daily was as effective as bendroflumethiazide 2.5 mg daily for maintenance treatment in mild to moderate congestive heart failure.

Adult↗

PubMed1981

Comparison of the effects of muzolimine and furosemide in patients with end-stage renal failure on chronic dialysis.

The pharmacodynamic effects of muzolimine and furosemide were compared in a single dose cross-over study in 8 patients on regular dialysis treatment, who had a residual diuresis of more than 300 ml/day. The study periods comprised two dialysis-free intervals of 3 days. On the second dialysis-free day either muzolimine 240 mg or furosemide 240 mg was administered orally. Urine was collected in 12-h periods on the pre-treatment, treatment and post-treatment days, and the excretion of sodium, potassium, urea and creatinine were measured. After administration of muzolimine 240 mg urine volume rose to twice that of the previous day, and sodium excretion increased approximately threefold. In contrast, the effect of furosemide 240 mg was not a pronounced; the diuresis was only 1.6 times that on the previous day and natriuresis was only 2.2 times as large. Excretion of potassium and creatinine was only slightly increased by either substance. The elimination of urea was increased by both substances to the same degree as the corresponding increase in diuresis.

Creatinine↗

PubMed1980

Effects of a new diuretic (piretanide) compared with furosemide on renal diluting and concentrating mechanisms in patients with the nephrotic syndrome.

The mode and site of action of the new diuretic agent piretanide were investigated in man. The effect of a single oral dose of 12 mg was compared with that of furosemide 80 mg p.o. iin 6 patients with the nephrotic syndrome. Piretanide showed a greater diuretic and natriuretic response than furosemide during maximal water diuresis, but the effect was similar in the hydropenic state. Like furosemide, piretanide decreased free water clearance relative to delivery during water diuresis and the reabsorption of solute-free water during hydropenia. This inhibitory action on both the concentrating and diluting urinary mechanisms demonstrates an effect of piretanide localized in the ascending limb of Henle's loop. Consistent alterations in glomerulur filtration rate, renal blood flow or filtration fraction were not observed.

Body Water↗

PubMed1984

Cytotoxic effect of choline, abolished by furosemide, in the diluting segment of frog kidney.

Previous observations suggest that luminal application of tetra-N-alkylammonium ions may impair ion transport in the amphibian diluting segment. To investigate this question conventional KCl-filled and Cl- sensitive microelectrodes were applied in diluting segments of the isolated perfused kidney of rana esculenta to evaluate transepithelial electrical and chloride electrochemical (PDte, EClte) as well as peritubular cell membrane potential difference (PDpt), measured at static head conditions. After determination of control values the tubule lumen was exposed to choline (95 mmol/l, substituted for Na+) both in presence or absence of furosemide (5 X 10(-5) mol/l). Then, the lumen was again perfused with control solution and the measurements were repeated. Thus, a time course for possible choline induced effects was obtained both in the presence and absence of furosemide. The lumen positive PDte decreased from 11.2 +/- 1.0 mV to 6.3 +/- 0.8 mV after 2 min and to 1.9 +/- 0.4 mV after 30 min exposure to choline. PDpt (cell interior negative) decreased from 70 +/- 2 mV to 58 +/- 3 mV and to 42 +/- 5 mV after 2 and 30 min, respectively. Intraluminal Cl- activity increased from its initial steady state value of 20 +/- 2 mmol/l to 39 +/- 2 mmol/l after 30 min exposure to choline. However, if the tubule lumen was exposed to choline in presence of furosemide (5 X 10(-5) mol/l), all the above described choline-induced effects did not become apparent.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1978

Pharmacokinetics of furosemide in gestosis of pregnancy.

Furosemid 50 mg was administered orally and intravenously to twelve gestotic women for brief periods as a part of a randomized, multicentre clinical trial comparing the efficacy of bed rest and pharmacological treatment. The pharmacokinetic profile was investigated using a gas-liquid chromatographic technique. The plasma half-life after oral and intravenous administration was 115 +/- 37.1 and 71.8 +/- 26.3 min and plasma clearance was 153 +/- 48 and 152 +/- 23 ml/min, respectively (mean +/- SD). Comparative data from healthy pregnant women cannot be obtained for ethical reasons. The results show that gestosis has only a marginal if any effect on the kinetics of furosemide in comparison with published kinetic parameters in healthy volunteers, and patients with renal failure. The new-born babies where checked for side effects according to a protocol in use in a larger regional surveillance programme. No clinical side-effects were attributable to furosemide, but the small size of the group does not permit any definitive conclusions about this aspect.

Administration, Oral↗

PubMed1992

Ethacrynic acid and furosemide alter Cl, K, and Na distribution between blood, choroid plexus, CSF, and brain.

Can loop diuretics like ethacrynic acid and furosemide, when administered intravenously, significantly alter ion transport and fluid dynamics in CNS? To shed light on this unresolved issue, we tested the ability of these agents to effect redistribution of Na, K and Cl in adult rat brain. Cl penetration into various CNS regions was assessed as the volume of distribution, i.e., uptake, of 36Cl from blood. Ethacrynic acid and furosemide (50 mg/kg IV) reduced by 20-30% the rate of permeation of 36Cl across the blood-CSF barrier, and they elevated [K] and [Cl] in choroid plexus (CP) by 15-25%. The loop diuretic-induced buildup of K and Cl in CP (lateral and 4th ventricle) was likely a reflection of decreased movement of these ions across the apical membrane into CSF. 36Cl activity in parietal cortex and pons-medulla decreased in treatment with furosemide and ethacrynic acid, due to slowing of Cl transport across blood-brain and/or blood-CSF barriers. Our inhibitory findings in intact rats are consistent with those from previous in vitro experiments demonstrating diminution by loop diuretics of Na, K and Cl transport across isolated CP membranes.

Acetazolamide↗

PubMed1983

Renal clearance of digoxin in man after sodium loading or furosemide treatment.

To evaluate the influence of different types of natriuresis on the renal clearance of digoxin (Cldig) and the Cldig/Clcr ratio, studies were performed in which sodium-depleted patients were placed on a moderately high sodium diet for 6 days. In another group natriuresis was evoked by furosemide. In the first study, in 10 patients, there was a 10-fold increase in Na excretion and a small rise in diuresis (V) and Clcr, which was accompanied by an increase in Cldig from 57.5 +/- 32, and 60.7 +/- 27.3 (duplicate measurements) to 103.9 +/- 55.4 (p less than 0.01) and 103.8 +/- 46.5 ml min-1 (p less than 0.01). Cldig/Clcr rose from 0.60 +/- 0.24 and 0.61 +/- 0.16 to 0.91 +/- 0.31 and 0.91 +/- 0.21, respectively (both p less than 0.005). Serum digoxin concentration declined from 1.24 +/- 0.35 and 1.19 +/- 0.40 to 1.02 +/- 0.35 and 0.97 +/- 0.32 micrograms/l (both p less than 0.01) during the high sodium diet. In the furosemide-induced natriuresis (6 patients), changes in Na excretion and V were a multiple of those caused by Na loading, but the Cldig/Clcr ratio was not increased. The results are in accordance with the concept of digoxin backdiffusion in the proximal tubules, which is dependent on proximal Na reabsorption. In the more distal segments of the nephron, where the action of furosemide occurs, there does not appear to be any transtubular movement of digoxin.

Creatinine↗

PubMed1988

Interaction between furosemide and the converting enzyme inhibitor benazepril in healthy volunteers.

Single oral doses of 10 mg converting enzyme inhibitor benazepril (CGS 14824A) and 40 mg furosemide were administered to 12 healthy male volunteers either separately or concomitantly. The pharmacokinetic parameters of benazepril were not influenced by coadministration of furosemide. Urinary excretion of total furosemide was significantly reduced by 10 to 20% in the presence of benazepril. This effect was considered clinically insignificant. Erect blood pressure decreased and pulse rate increased only during concomitant treatment.

Adult↗

PubMed1989

Furosemide pharmacokinetics and pharmacodynamics in health and disease--an update.

The literature on furosemide pharmacokinetics and pharmacodynamics is critically reviewed, concentrating on those papers published subsequent to the 1979 reviews of this topic. Intravenous and oral data are presented for healthy volunteers and for patients with various disease states. It is the latter populations about which the majority of the studies have been published since 1979. Inter- and intraindividual variations in bioavailability are discussed, as are data on the metabolism of furosemide to its glucuronide conjugate. Published studies examining the relationship between furosemide pharmacodynamics and pharmacokinetics are also evaluated. The literature is reviewed through June 1988.

Disease↗

PubMed1986

Effects of the rate and composition of fluid replacement on the pharmacokinetics and pharmacodynamics of intravenous furosemide.

Effects of differences in the rate and composition of intravenous fluid replacement for urine loss on the pharmacokinetics and pharmacodynamics of furosemide were evaluated using the dog as a model animal. Each of six dogs received 8-hr constant intravenous infusion of 20 mg (15 mg used in one dog) of furosemide with 0% replacement (treatment I), 50% replacement (treatment II), and 100% replacement (treatment III) with lactated Ringer's solution, as well as with 100% replacement with 5% dextrose in water (treatment IV). Most pharmacokinetic parameters, such as plasma clearance, steady-state volume of distribution, mean residence time, and terminal half-life, were essentially the same in all four treatments. Renal clearances and urinary excretion rates of the drug in treatments II-IV were essentially the same, but about 20% higher than those in treatment I. In spite of the similarities in kinetic properties, diuretic and/or natriuretic effects from furosemide were markedly different among the four treatments. For example, mean 10-hr urine outputs were 646, 1046, 3156, and 1976 ml and mean 10-hr sodium excretions were 87.0, 142, 383, and 97.2 mmole for treatments I-IV, respectively. Except for treatment III, diuresis and/or natriuresis were found to be time-dependent, generally decreasing with time until reaching a low plateau during later hours of infusion. The present findings also showed that no fluid replacement and 100% replacement with 5% dextrose solution both produced the same degree of severe acute tolerance in natriuresis, indicating the insignificance of water compensation in tolerance development; in treatment II, where neutral sodium balance was achieved, the development of acute tolerance in diuresis and natriuresis can mainly be attributed to negative water balance under this special condition; at steady state the hourly diuresis and natriuresis could differ up to about ten times between treatments. Some implications for the kinetic/dynamic relationship or modeling, in the clinical use, and in the bioequivalence evaluation of dosage forms are discussed.

Animals↗

PubMed1975

[Age-dependent biochemical studies on the extrarenal effect of furosemid (author's transl)].

The present study investigated the activities of lysosomal enzymes of the liver after administration of Furosemid. 10 weeks and 1-year old male albino rats were treated with 40 mg Furosemid for 4 subsequent days. According to the method devised by de Duve a sediment rich in lysosomes was produced by fractionated centrifugation and subsequently the enzyme activity of beta-glucuronidase, beta-acetylglucosaminidase, cathepsin D and a collagenolytic enzyme was measured in the sediment as well as in the corresponding lysosomal supernatant. The protein content served as a reference for the enzyme activities. In addition, we investigated the activities of cytoplasmic enzymes such as GOT, GPT, gamma-GT and the alkaline phosphatase. The enzyme activity changes were age-dependent. With Furosemid treatment the activities of beta-glucuronidase and cathepsin D increased in the lysosomal supernatant and the lysosomal sediment of the 1-year old rats, whereas the activities of the collagenolytic enzyme increased in the lysosomal sediment of the same group. In the lysosomal sediment of the 10-weeks old rats a decrease of beta-glucuronidase, beta-acetylglucosaminidase and cathepsin D was observed. These results are discussed in the light of reports from the literature.

Age Factors↗

PubMed1987

Effect of membrane potential on furosemide-inhibitable sodium influxes in human red blood cells.

Furosemide-inhibitable Na influx (a measure of Na/K/Cl cotransport) was determined as a function of membrane potential in human red blood cells. The membrane potential was varied from -42 to +118 mV using valinomycin and gradients of K. The furosemide-inhibitable, unidirectional Na influx was independent of membrane potential over the entire range of potentials. The change in flux per mV, 0.443 mumol/(liter cells.hr.mV), was not significantly different from zero. The mean flux was 153 +/- 16 mumol/(liter cells.hr) (+/- SEM, n = 71). The ouabain and furosemide-resistant influxes of Na and K were also measured as functions of membrane potential using either valinomycin and K or a chloride-free, tartrate flux medium to vary membrane potential. The unidirectional Na influx decreased slightly as the membrane potential was increased from negative potentials to about +10 mV. At higher membrane potentials Na influx rose dramatically with potential. This increase was not reversible and was also observed with K influx.

Adult↗

PubMed1982

Determinants of the diuretic response to furosemide in infants with congestive heart failure.

A wide interindividual variation in the degree of diuresis produced following treatment with furosemide has been observed in infants with congestive heart failure. A method of pharmacokinetic analysis that separates drug disposition from renal response to furosemide was used to compare the effect of this agent in infants with congestive heart failure with the effect seen in infants with fluid retention secondary to noncardiac factors. No differences in the drug elimination rate, urinary drug excretion, or renal diuretic response between the 2 groups were seen. Infants in both groups exhibited a wide range in all variables examined. The marked interindividual variation in response originates from decreased delivery of furosemide to its site of action in some patients and a decreased responsiveness to the drug in others.

Diuresis↗

PubMed2002

Is furosemide administration effective in improving the accuracy of determination of differential renal function by means of technetium-99m DMSA in patients with hydronephrosis.

It has been suggested that determination of differential renal function (DRF)using technetium-99m dimercaptosuccinic acid (DMSA) may lead to overestimation of the function of an obstructed kidney in patients with excretion abnormalities owing to pelvic retention of DMSA. Recently published guidelines have recommended use of furosemide injection when calculating DRF in these particular patients. The aim of this study was to evaluate the effect of diuretic administration on the determination of DRF using DMSA scintigraphy. For this purpose, 19 patients, aged from 1 month to 69 years (19.4+/-24.8 years, 15 males, 4 females), in whom pelvic retention had been documented by diuresis scintigraphy were included in the study. DMSA scintigraphy was performed in all patients 2-4 h after injection and six planar images were obtained. Immediately after the standard study, furosemide was injected in all patients, and 30 min later the same number of images was obtained. DRF was calculated for each patient and from each DMSA study by using the arithmetic mean method. The difference between two studies (DMSA scintigraphy with or without furosemide administration and diuresis scintigraphy) was expressed as a percentage of the mean value of the two studies (the DRF value of the affected kidney was thus taken into account). The mean of the differences represented the systemic bias and the SD of the mean of the differences represented the precision of the technique. In seven patients, diuresis renography revealed an obstructive curve pattern. We did not observe any significant difference between the DRF values obtained before and after diuretic administration ( P>0.5). When we compared DRF values obtained from standard and from diuretic DMSA studies, the mean of the differences was only 0.3% and the SD was only 1.2%. There was also no significant difference in DRF between patients with the obstructive curve pattern and those with a dilated renogram curve pattern (with washout of activity during the second phase of the study) ( P>0.1). In conclusion, we did not observe interference from pelvicalyceal activity in patients with documented pelvic retention and infer that diuretic administration may be a useless intervention for improving the accuracy of determination of DRF.

Adolescent↗