Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FUROSEMIDE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 919 records · Page 51Linked to original sources
PubMed1992

External-standard high-performance liquid chromatographic method for quantitative determination of furosemide in plasma by using solid-phase extraction and on-line elution.

A rapid and simple external-standard high-performance liquid chromatographic (HPLC) method has been developed for the determination of the concentration of furosemide in plasma. The analyte is extracted with a C-2 ethyl sorbent. On-line elution of the analyte into the HPLC system is accomplished with an advanced automated sample processor (Varian). Furosemide is quantified by fluorescence detection within a linear range of 25 to 1000 ng/mL (average correlation coefficient, 0.9998), with a limit of detection of 1.8 ng/mL. Both internal- and external-standard procedures were evaluated, and the external-standard procedure demonstrated superior characteristics. The external-standard procedure was precise to within a relative standard deviation of 8% and accurate with less than 3% error throughout the concentration range studied. The external-standard HPLC method was used to analyze the concentration of furosemide in greater than 1000 plasma samples obtained from patients with either normal kidney function or renal failure who had received furosemide either orally or intravenously in an experimental setting.

Aged↗
PubMed2000

Thiamin status in furosemide-treated rats.

Rats were treated with furosemide at intraperitoneal doses of 10, 20, and 30 mg kg(-1)day(-1)for 21 days, and some indices of thiamin status (liver, blood and urine thiamin concentrations, erythrocyte transketolase (TK) activity, and thiamin pyrophosphate (TPP) effect, which refers to the increase in TK activity in a deficient haemolysate due to the addition of TPP before incubation) were measured. The results indicated that, at doses of 20 and 30 mg kg(-1)(but not 10 mg kg(-1)), furosemide produced significant effects on these indices suggestive of thiamin deficiency. In another experiment, the effect of thiamin treatment (20 and 100 microg kg(-1)) in rats concomitantly given furosemide (30 mg kg(-1)) was investigated. The high dose of the vitamin was sufficient to overcome the biochemical signs of thiamin deficiency induced by furosemide.

Animals↗
PubMed1988

Short-term stimulation of cellular autophagy by furosemide in the thick ascending limb of Henle's loop in the rat kidney.

In an effort to investigate the functional relationship between cell-specific work and intracellular degradative processes, the effect of furosemide on cellular autophagy was investigated in two different portions of the nephron, namely, the thick ascending limb of Henle's loop (TAL), which is a main target of this drug, and the proximal convoluted tubule (PCT) as a reference structure. Eight male adult rats were treated with furosemide (60 mg/kg body weight, s.c.). Eight control animals received physiological saline. 1 to 4 h after the injections the animals were killed by perfusion fixation. Small specimens of kidney tissue from the inner stripe of the outer medulla and from the outer cortex were processed for electron microscopy; they were investigated morphometrically for volume fraction and numerical density of autophagic vacuoles (AVs). A significant increase of both parameters (volume fraction: 0.42 x 10(-4) to 1.09 x 10(-4); numerical density: 4.2 x 10(5)/mm3 to 15.5 x 10(5)/mm3) was seen under the influence of furosemide in TAL cells, whereas PCT cells did not show a significant increase in volume fraction or any increase in numerical density of AVs. These data suggest that the functional unloading of TAL, via blocking of the Na+-2Cl- -K+ co-transport by furosemide, results in adaptative "structural unloading", i.e., an increased sequestration of cytoplasmic components into AVs, within a short-time interval.

Animals↗
PubMed1989

Evaluation of the effect of furosemide on ultrafilterable platinum kinetics in patients treated with cis-diamminedichloroplatinum.

It has been reported that furosemide can prevent platinum nephrotoxicity by dilution of the toxic drug in the tubule or by another unknown mechanism. To evaluate its influence on ultrafilterable platinum pharmacokinetics, we undertook a randomized prospective trial of cis-diamminedichloroplatinum (CDDP) (80 mg/m2 by a 20-min infusion) administered to 20 patients with hydration-induced diuresis. Ten patients received 20 mg/m2 furosemide 1 h before CDDP administration, and 10 patients received no diuretic drug. Plasma and urinary pharmacokinetics of platinum and creatinine were compared in both groups of patients. Plasma total and ultrafilterable platinum was always higher in the furosemide group. However, protein binding, urinary concentrations, cumulative urinary excretion, renal clearance and creatinine clearance/renal clearance ratio (fractional clearance) were not statistically different. Moreover, the fractional clearance was successively lower, equal and higher than one in both groups. These results suggest that: (1) furosemide probably causes water depletion leading to a rise in plasma concentrations; (2) its protection by a pharmacokinetic interaction is doubtful, since all other parameters (especially urinary parameters) are not significantly modified; (3) renal clearance and fractional clearance suggest a bidirectional transport of platinum in the tubule not influenced by the diuretic drug.

Cisplatin↗
PubMed1991

Response to furosemide during dehydration with and without naproxen pretreatment of kidney donors and renal transplant recipients.

The response to 40 mg furosemide p.o. in 6 healthy kidney donors and 6 renal transplant recipients with and without naproxen pretreatment has been studied. No volume replacement was given in order to study the development of tolerance. The subjects showed an average dehydration of 1.5 kg.6 h-1. While mean creatinine clearance was equal in patients and donors (76 vs 80 ml/min), renal furosemide clearance was significantly lower in the patients (47 vs 81 ml min; P less than 0.05). The patients also excreted a smaller fraction of the dose in the urine (5.7 vs 7.8 mg/6 h; P less than 0.05). As the overall renal sensitivity was similar in the two groups, the natriuretic response was correspondingly smaller in transplant recipients as compared to donors. Within the observation period of 6 h after dosing, acute tolerance developed in the donors and in 4 of the 6 patients, as shown by clockwise hysteresis in the dose (urine furosemide excretion rate)-response (natriuresis) curves. Pretreatment with naproxen reduced renal sensitivity to furosemide (right shift of the dose response curve) in all the donors but in only 2 of the patients. In both groups acute tolerance was less pronounced after naproxen, which may indicate involvement of the prostaglandin system in the development of acute tolerance. The results may also indicate regeneration of sympathetic nerves with functional capacity in at least some renal transplants, or that other mechanisms of salt regulation compensate for loss of sympathetic nerve activity.

Administration, Oral↗
PubMed1975

Effects of furosemide on sodium content and transport pool in frog skin (Rana esculenta): comparison with vasopressin and ouabain.

The effects of ouabain, vasopressin, and furosemide on intracellular concentrations of total sodium([Na]) and potassium [K]), on exchangeable sodium ([Na]) and the sodium transport pool ([Nap]) were investigated in isolated short circuited skins of rana esculenta. Furosemide was added to the epithelial bathing solution, vasopressin and ouabain to the corial bathing solution. Results were compared with the amount of net sodium transport measured by short circuit current (scc). Ouabain reduces scc and increases [Na] and [Na]; [K] is decreased. The administration of vasopressin leads to a sharp increase of scc, combined with an enhancement of of [Na] and [Na]; [K] shows no significant change. [Nap] is significantly increased, too, and approximately to the same amount as [Na]. Furosemide causes an increase of scc, whereas a significant change of [Na], [Na] and [K] could not be detected. On the other hand, [Nap] was enhanced significantly. The results support the hypothesis that furosemide like vasopressin is acting by increasing the entry of sodium into the transport compartment of the active cell layer. The result is an increased transfer of sodium across the skin.

Animals↗
PubMed1984

Comparison of the short-term effects of the loop diuretic piretanide and furosemide in patients with renal insufficiency.

The natriuretic effect of the new loop diuretic piretanide was investigated in patients with severe renal insufficiency and was compared with that of furosemide. In the first study 4 hospitalized patients (serum creatinine 407 to 1220 mumol/l) were examined after administration of piretanide (12, 24, 48 and 96 mg to two patients, and 24, 48, 96 and 192 mg to 2 other subjects, given every third day). In the second study 6 hospitalized patients (serum creatinine 194 to 698 mumol/l) were studied after receiving orally 2 different doses of piretanide and 2 different doses of furosemide orally, given every fourth day. The mean natriuretic effect of 48 mg and 96 mg piretanide was 250 and 340% of the control value for the entire group, and 311 to 480% in the subgroup of patients with serum creatinine below 530 mumol/l. For a given dose the natriuresis was inversely correlated with renal function, and at a given serum creatinine level the natriuretic response was dose-dependent. The drug had less effect on water and potassium diuresis than on natriuresis. No significant difference in natriuretic effect was found on comparison with furosemide given in the ratio furosemide:piretanide 3.33:1. The pharmacokinetic data showed a direct correlation between the dose and the mean plasma concentration and also between urinary recovery of the drug and the measured natriuretic response.

Creatinine↗
PubMed1987

Plasma protein binding of furosemide in the elderly.

The protein binding of furosemide was investigated in plasma from 22 old and 11 young subjects by equilibrium dialysis. The unbound fraction of furosemide was 3.16% in plasma from the elderly and 1.7% in plasma from the young. A significant correlation was found between the unbound fraction of furosemide and the plasma concentration of albumin. The average number of binding sites was 3.8 (elderly) and 2.7 (young) 10(-6) mol/g albumin. The average association constant (K) was 4.3 (elderly) and 4.2 (young) 10(5) M-1. By increasing the concentration of furosemide up to 200 micrograms/ml buffer the unbound fraction of the drug rose to 5.2% (elderly) and 3.5% (young).

Adult↗
PubMed1984

Implications of intraindividual variability in bioavailability studies of furosemide.

Intrasubject variation in bioavailability (rate and extent) and disposition of furosemide 40 mg was investigated using a repeated, randomized, double-blind cross-over study in 8 healthy subjects. Two generic tablet formulations (Lasix and Furix) and intravenous furosemide were compared on 6 separate days. Extensive intrasubject variability after oral administration was observed in AUC, mean absorption time (MAT) and urinary excretion. The variability (error variance) within the dosage forms was as large as that between the two generics. These variations most probably depended on the absorption process, since the repeated i.v. doses showed only marginal intrasubject variability. Absolute bioavailability was 56% for Lasix and 55% for Furix (AUC). The range was 20 to 84% between individuals and the maximal range within one individual was 20 to 61%. Confidence interval and Bayesian analysis showed a high probability of non-equivalence not only between but also within the generics when the separate cross-over experiments were analyzed (8 observations). When extending the analysis to 16 observations, bioequivalence was demonstrated for the two generic tablets. Rate of absorption, quantified as MAT, was 128 min for Lasix and 98 min for Furix (16 observations). Since MAT was significantly longer (p less than 0.001) than the mean residence time after the i.v. dose (57 min), absorption was evidently the rate-limiting step in the overall kinetics of oral furosemide. Intraindividual variation in absorption is a confounding factor in bioavailability studies of furosemide using limited numbers of subjects. This is important to consider when designing and evaluating bioavailability studies for drugs showing these variations.

Administration, Oral↗
PubMed1977

Comparison of the pharmacodynamic effects of furosemide and BAY g 2821 and correlation of the pharmacodynamics and pharmacokinetics of BAY g 2821 (muzolimine).

In a biometrically planned, double-blind study on 12 Oedema-free male patients the saluretic effect of muzolimine 30 mg was compared with furosemide 40 mg. The plasma level of muzolimine was determined and correlated with its pharmacodynamics. In terms of excretion during the 12-hour observation period muzolimine 30 mg had as great a cumulative effect as furosemide 40 mg. There was a significant difference in the time-response curve. During the first gwo hours furosemide 40 mg had more saluretic effect than muzolimine 30 mg. Between two and four hours there was no significant difference between the two substances. Between four and six hours, however, muzolimine was somewhat more effective than furosemide, although the difference did not reach the level of significance. After 6 h there was no longer any difference between the two compounds. The half-life of the fall in concentration of muzolimine in plasma was 3.7 up to 10 h after its administration. The time-response curve of the increased urine excretion correlated well with the time course of the concentration of muzolimine in plasma.

Adult↗
PubMed1981

Effect of calcium, furosemide and chlorothiazide on net volume reabsorption and basolateral membrane potential of the distal tubule.

In the distal tubule of the isolated kidney of Amphiuma net volume reabsorption (split-oil droplet method) and basolateral membrane potential (psi b) were measured. Luminal perfusion solution could be changed rapidly from 108 mmol . 1-1 NaCl plus 0.1 mmol . 1-1 calcium to solutions containing 103 or 97 mmol . 1-1 NaCl plus 3.6 or plus 7.2 mmol . 1-1 calcium. Furthermore, 10(-4) mol . 1-1 furosemide or chlorothiazide were applied luminally. (1) Addition of 7.2 mmol . 1-1 calcium hyperpolarized psi b from -73.4 mV to -108.3 mV and inhibited net volume reabsorption. (2) Similarly, when furosemide was injected, psi b was hyperpolarized and net volume reabsorption reduced. Application of both high calcium and furosemide further inhibited volume reabsorption. (3) The effects of chlorothiazide were similar to those of furosemide. However, when both high calcium and chlorothiazide were administered psi b and volume reabsorption were almost normalized. (4) The data are consistent with the hypothesis that calcium and the diuretics interfere primarily with chloride uptake across the luminal membrane and thus reduce sodium chloride transport. When chlorothiazide in the presence of high luminal calcium almost normalized chloride transport, it is likely that its effects were by stimulating calcium transport and thus increasing intracellular calcium activity.

Animals↗
PubMed1986

Blockage of Ca-activated Cl conductance by furosemide in rat lacrimal glands.

Single cells isolated from rat lacrimal glands were studied with the tight-seal whole-cell recording technique. It was found that furosemide (1 mM, applied externally) selectively blocked one part of the electrical response elicited by muscarinic agonists. This component of the response had been shown in a previous work (Marty et al. 1984) to be due to Ca-dependent Cl channels. The action of furosemide was further studied on cells which were dialysed with a high-Ca, high-Na solution, and which mainly displayed the Ca-dependent Cl conductance. In these experiments, furosemide (1 mM) was again found to depress the Ca-dependent Cl current. The present findings offer an explanation for previous reports that furosemide blocks ion fluxes and electrolyte secretion in exocrine glands without necessarily involving the neutral Na-K-Cl carrier usually assumed to be affected by the drug.

Animals↗
PubMed1976

Renal effects of furosemide in glycerol induced acute renal failure of the rat.

The renal effects of furosemide in acute renal failure of the rat were studied using clearance and micropuncture techniques. Acute renal failure was induced by an intramuscular injection of 50% glycerol (10 ml/kg). Functional impairement of the glycerol treated animals consisted of a decrease in urinary sodium excretion, renal blood flow, total kidney GFR and effective filtration pressure of superficial nephrons. Effective filtration pressure was calculated from proximal free flow and stop flow pressure measurements. In contrast to control animals furosemide did not increase urine volume during acute renal failure due to a marked fall in GFR. Renal blood flow, as measured by an electromagnetic flowmeter, also decreased after furosemide in glycerol treated rats and increased in control animals. Furosemide reduced effective filtration pressure during acute renal failure to almost zero, whereas in control animals effective filtration pressure virtually remained constant.

Acute Kidney Injury↗
PubMed1986

The influence of furosemide and Co2+ on electrolyte and water transport in newt distal tubule and frog skin.

The technique of stationary microperfusion of the early distal tubule used in experiments on male newts (Triturus vulgaris) revealed the intratubular effect of CoCl2 and furosemide on the ion transport. CoCl2 in concentration 5 X 10(-4) M increased Na and Cl reabsorption, reduced Ca, Mg and K reabsorption, and increased (TFexp/TFo)in from 1.14 +/- 0.04 to 1.68 +/- 0.27 (p less than 0.001). CoCl2 in concentration 5 X 10(-5) M enhanced Na and Cl reabsorption, without affecting transport of other ions. 6 X 10(-4) M furosemide decreased reabsorption of water, Na, Cl, Ca and Mg. The combined effect of Co2+ and furosemide inhibited reabsorption of Mg and Ca to a greater extent, but stimulated Na reabsorption. Experiments on frog skin showed that being added to the apical membrane of cells, Co2+ stimulates short circuit current and potential differences, whereas furosemide reducing Cl absorption induces only hyperpolarization. Experimental findings allow to assume that Co2+ on the outer surface of the apical membrane of the distal tubule cells blocks the selective Ca and Mg channels and activates Na channels.

Animals↗
PubMed1993

Assessment of high-energy phosphorus compounds in the rat kidney by in situ 31P nuclear magnetic resonance spectroscopy: effect of ischemia and furosemide.

31P nuclear magnetic resonance (NMR) spectroscopy of the in situ rat kidney was performed by a surface coil method, and the effects of ischemia and furosemide infusion were assessed. 31P NMR spectra of the kidney subjected to 30 min of ischemia returned completely to the pre-ischemic level after 60 min of reperfusion. But the 31P NMR spectra after 60 min of ischemia did not recover, even after 120 min of reperfusion. Levels of beta-ATP and inorganic phosphate (Pi) decreased and the chemical shift of Pi increased after intravenous infusion of furosemide. This increase in chemical shift might signal an alkalotic change in intracellular pH. Furosemide infusion prior to ischemia is thought to protect the kidney from injury induced by 60 min of warm ischemia. The chemical shift of Pi returned to the pre-ischemic level earlier than beta-ATP and Pi. In conclusion, according to the findings of 31P NMR spectroscopy, furosemide infusion prior to ischemia may be effective in protecting the kidney against ischemic injury. But the change in Pi peak and the causes of the dissociation of Pi and beta-ATP should be examined further.

Animals↗
PubMed1983

Diuretic effect of slow-release furosemide in elderly patients.

To compare the natriuretic and diuretic effects of a slow-release and a standard formulation of furosemide, 18 elderly patients with stable congestive heart failure were hospitalized and treated with one of these formulations in a double blind randomized trial. Patients received placebo on the first 2 days, furosemide on the third day and placebo again on the last 2 days of the study. In patients receiving the standard formulation mean urine output was increased only on the day of active treatment. However, in patients who had received the slow-release preparation, increased urine excretion was seen both on the day of active treatment and on the subsequent day. The total diuresis (0-48 h) in the 2 groups was equal, but a peak diuresis (0-6 h) was seen only in patients on the standard formulation of furosemide. Sodium excretion followed the pattern of urine excretion. Furosemide in a slow-release formulation offers advantages in maintenance therapy in congestive heart failure, especially in elderly patients.

Aged↗
PubMed1975

Furosemide, mithramycin, and salmon calcitonin in hypercalcemia.

Twenty-nine patients with acute hypercalcemia secondary to carcinoma, myeloma and parathyroid adenoma have been treated with large doses of furosemide, mithramycin, or salmon calcitonin perfusion. With furosemide administration the treatment was successful in 6 of 10 patients. Furosemide was injected intravenously at the rate of 125 mg every 3 hours. With mithramycin perfusion only 2 of 8 patients have a return of the serum calcium levels to normal. With salmon thyrocalcitonin 3 of 10 patients obtained a good result. It can be interesting to suggest the association of furosemide and salmon calcitonin infusion to treat hypercalcemia of myeloma.

Adenoma↗
PubMed1985

Quantitative evaluation of ototoxic side effects of furosemide, piretanide, bumetanide, azosemide and ozolinone in the cat--a new approach to the problem of ototoxicity.

A new method for the quantitative assessment of acute ototoxic side effects of drugs is described. It is suitable for screening purposes. The method is based on the determination of the toxic dose (TD50) which causes a defined hearing loss in 50% of the animals tested. The hearing loss is defined as a complete suppression of the compound action potential (CAP) of the auditory nerve, elicited by clicks 30 dB above threshold. This is approximately equivalent to a clinical hearing loss of 30 dB. The TD50 is used to estimate the therapeutic range. With this approach ototoxic side effects of furosemide, piretanide and bumetanide were compared quantitatively in cats. The TD50 values for CAP suppression were 18.37 mg/kg for furosemide; 4.29 mg/kg for piretanide and 2.21 mg/kg for bumetanide. As equipotent diuretic doses are 2.61 mg/kg for furosemide, 0.26 mg/kg for piretanide and 1.16 mg/kg for bumetanide, it appears that the relative ototoxicity is least for piretanide and highest for bumetanide. Plasma concentrations, determined initially and when recovery of CAP to 50% of control had occurred, indicate that bumetanide may be more slowly eliminated from the cochlear spaces than furosemide and piretanide. In addition azosemide and ozolinone were tested. The TD50 for azosemide was less than 10 mg/kg. With ozolinone where there are two isomers, only the diuretic (-)ozolinone was ototoxic; the TD50 was less than 100 mg/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗