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PubMed2000

Preparation and characterization of Furosemide-Eudragit controlled release systems.

Solid dispersions and physical mixtures were prepared and characterized by X-ray diffraction, infrared spectroscopy, electronic microscopy and dissolution rate studies. The characterization with X-ray diffraction showed a transition from the crystalline to the amorphous phase. A new phase near 50% Furosemide concentration with both types of carriers was present. From infrared spectroscopy strong interactions between amine and carbonyl groups from both the Furosemide and the polymers were found. Electronic microscopy analysis showed that the Furosemide changed its crystalline habit from needle to a new spherical phase, with diameter near to 1 microm. Solid dispersions were prepared in order to modify the system characteristics. The Furosemide dissolution rate was determined in order to follow the behavioural changes of the system. Scanning electron microscopy showed the presence of micro spheres within the polymeric matrix, and the channels formed due to the Furosemide dissolution inside the Eudragit: this fact modified the release pattern of the Furosemide system.

Acrylic Resins↗
PubMed1997

Effect of inhaled furosemide and cromolyn on bronchoconstriction induced by ultrasonically nebulized distilled water in asthmatic subjects.

BACKGROUND: Inhaled furosemide has been shown recently to produce a protective effect against bronchoconstriction induced by several indirect stimuli, including ultrasonically nebulized distilled water (UNDW). Since there is a close parallel between its experimental effects and those reported for cromolyn,/it has been suggested that they may share some common mechanisms of action. Their protective effect, however, has never been compared directly. In this study, therefore, we have investigated the ability of equal doses (30 mg) of inhaled furosemide and cromolyn to modulate bronchoconstriction induced by UNDW in a group of ten asthmatic patients. METHODS: Subjects with documented bronchial response to UNDW were enrolled in a randomized, double-blind, placebo-controlled study. Treatments were administered five minutes prior to increasing outputs of UNDW and the response was expressed as the provocative output causing a 20% fall in FEV1 (PO20, in mL/min) and as the output-response slope. RESULTS: Geometric mean PO20 increased from 1.53 to 4.05 mL/min (P < .0004) after furosemide. After inhaling the highest output of UNDW (5.2 mL/min), PO20 was not measurable in six of ten patients when pretreated with furosemide and in all patients when pretreated with cromolyn. This difference was statistically significant (P < .05). Geometric mean values of output-response slope significantly decreased from 13.6 to 2.97 after furosemide (P < .0001) and from 13.6 to 1.43 (P < .0002) after cromolyn. CONCLUSIONS: These results suggest that cromolyn has a slightly greater anti-reactive activity in UNDW-induced bronchoconstriction compared to furosemide.

Administration, Inhalation↗
PubMed1996

The renal clearance of unchanged cisplatin during furosemide and mannitol diuresis is dependent on glomerular filtration rate in rats.

The disposition of unchanged cisplatin (CDDP) in plasma and urine after bolus injection of CDDP (5 mg/kg) was compared in rats treated with furosemide (25 mg/kg as a 40-min iv infusion) and mannitol (2 g/kg as a 40-min iv infusion). Forced diuresis significantly increased renal clearance (Clr) of unchanged CDDP in the first 10-min period after CDDP administration, compared to that in the rats given CDDP alone. Compared with furosemide, mannitol showed greater modification in Clr of unchanged CDDP in the early phase and more accelerated urinary excretion of unchanged CDDP during the study. Furosemide increased plasma concentration and reduced urinary excretion of unchanged CDDP in the terminal phase. Clr of unchanged CDDP was found to be dependent of glomerular filtration rate (GFR) during diuretic coadministration. Linear relationships among urine flow rate, GFR, and Clr of unchanged CDDP were observed only in diuretic-treated rats. Although the relationships between GFR and Clr were almost identical, there was a difference in the GFR-urine flow rate relationship between furosemide- and mannitol-treated rats. GFR was gradually reduced during diuretic treatment, and furosemide induced greater GFR reduction than mannitol. This resulted in a modification of unchanged CDDP disposition by furosemide in the terminal phase. The present study suggests that careful monitoring and maintaining of GFR during coadministration of diuretic may be useful for predicting the urinary excretion behavior of unchanged CDDP in CDDP chemotherapy.

Animals↗
PubMed2004

[Fatal untoward effect of furosemide: immunocytopenic purpura and cerebral hemorrhage].

A 74 year old man was admitted to the hospital for purpura. The history revealed coronary heart disease. Bypass surgery had been performed 18 months ago. Furosemide had recently been prescribed for cardiac insufficiency and the patient had taken the drug intermittently over two weeks. Laboratory analysis showed severe thrombocytopenia. Despite immediate treatment with intravenous prednisolone and platelet transfusions the patient succumbed to cerebral hemorrhage. Autopsy confirmed a diffuse hemorrhagic diathesis and a cellular response of the bone marrow typical for an acute immune reaction. The start of the purpura nine to ten days after the first dose of furosemide, the exclusion of other possible causes for purpura and the focal proliferation of T-lymphocytes in the bone marrow render it highly probable, that furosemide was responsible for the fatal thrombocytopenia. Furosemide is discussed to have a potential for autoimmunological untoward effects due to its sulfonamide structure. Few case reports describe vasculitic and allergic phenomena. The generation of antibodies against thrombocytes and the depression of megakaryocytic function are thought to be involved. Our patient had been treated with furosemide during the bypass surgery 18 months before the development of purpura. A sensitization to furosemide probably took place at that time.

Aged↗
PubMed1988

Increased nonrenal clearance and increased diuretic efficiency of furosemide in cystic fibrosis.

The pharmacokinetics of furosemide and its diuretic effect were studied in six patients with cystic fibrosis (CF) and in six age-matched healthy volunteers. Furosemide was given intravenously at a dose of approximately 0.5 mg/kg. Renal excretion of furosemide was decreased in CF because nonrenal clearance was more than twice as high as in controls (p = 0.03). Nonrenal clearance correlated with the volume of distribution (r2 = 0.52, p = 0.01), which makes a difference in the distribution and binding determinants for clearance. Another reason for increased nonrenal clearance could be induction of drug metabolism in CF, but the excretion of furosemide conjugate did not differ significantly between the groups. Although 26% less furosemide was excreted in CF than in controls (p = 0.03), the diuretic response (calculated as excretion of water and electrolytes) did not differ. Thus the diuretic efficiency was higher in CF for Na+ (p = 0.02), Cl- (p = 0.01), K+ (p = 0.07), and volume (p = 0.005). This difference is probably secondary to the different rates of delivery of furosemide into urine.

Adolescent↗
PubMed1992

Diuretic efficiency of furosemide during continuous administration versus bolus injection in healthy volunteers.

Furosemide delivery rate in the nephron has been reported to be one of the major determinants of diuretic response. In a randomized, crossover double-blind study in eight healthy volunteers, we tested this hypothesis by comparing continuous intravenous infusion of furosemide (infusion rate, 4 mg/hr) during 8 hours after administration of an intravenous loading dose of 8 mg (total dose, 40 mg) with an intravenous bolus injection of 40 mg furosemide. During the study days subjects were rehydrated with isovolumetric amounts of fluid. Mean total urinary volume (Vur), sodium (UNa), potassium, and chloride excretion after 8 and 24 hours were significantly greater after treatment with continuous furosemide infusion when compared with bolus injection, whereas total urinary furosemide excretion showed no differences (Vur bolus versus Vur infusion, 5270 versus 6770 ml/8 hours; UNa bolus versus UNa infusion, 314 versus 430 mmol/8 hours; both p less than 0.001). These findings strongly support the concept of the furosemide delivery rate into the nephron as a determinant of diuretic efficiency.

Adult↗
PubMed1975

Effects of furosemide on low-dose mercuric chloride acute renal failure in the rat.

The use of potent diuretics in acute renal failure remains controversial. Both beneficial and detrimental effects have been reported. In the present study, the effects of both low and high doses of furosemide administered in the developmental and established stages of mercuric chloride-induced acute renal failure were evaluated. Both low and high doses of furosemide produced a significant diuresis when given early in the course of experimental acute renal failure. Despite this diuresis, furosemide did not modify the development of the acute renal failure. Continued administration of a low dose of furosemide had no effect on renal function; however, prolonged administration of high doses of furosemide resulted in significantly lower creatinine clearances 48 hr after induction of acute renal failure. This detrimental effect was due to sodium depletion by the diuretic since it was prevented by continuous replacement of urinary sodium losses. In the absence of sodium depletion, high doses of furosemide produced a significant diuresis, both in the developmental and established phases of acute renal failure, but it had no effect on the degree of renal functional impairment.

Acute Kidney Injury↗
PubMed1979

Synergism of dopamine plus furosemide in preventing acute renal failure in the dog.

The protective effects of a combination of dopamine and furosemide were studied in dogs during the initial phase of acute renal failure (ARF) induced by intravenous uranyl nitrate (10 mg/kg). Fifteen minutes after injection of the nephrotoxin, and infusion of dopamine (3 micrograms/kg/min), furosemide (1 mg/kg/bolus followed by 1 mg/kg/hr), or both drugs simultaneously were given for 6 hours. Exogenous creatinine clearance was measured for 6 hours, and the intrarenal blood flow was measured with radioactive microspheres before and 3 hours after the induction of ARF. Treatment with both dopamine and furosemide produced renal vasodilatation, high urine flow rate, and attenuation of the fall in GRF seen in untreated animals. In contrast, single use of dopamine or furosemide was totally ineffective in producing renal vasodilation, a diuresis, or the maintenance of the GFR. These data indicate that dopamine plus furosemide have a synergistic effect in preventing the early pathophysiologic changes associated with ARF in this animal model. Maintenance of a high GFR correlated best with the enhancement of solute excretion and urine flow rate. Potential protective effects of dopamine plus furosemide in other models of ARF deserve careful investigation.

Acute Kidney Injury↗
PubMed1982

Absorption and disposition of furosemide in congestive heart failure.

Changes in response to furosemide and other diuretics in patients with congestive heart failure (CHF) could occur because of disease-induced changes in absorption of the drug or changes in disposition which affect its access to its site of action. A difference was not found in the bioavailability of forosemide in patients with CHF compared to normal volunteers, 31 +/- 12 vs. 38 +/- 20% (mean +/- sd), respectively. Both groups showed considerable interindividual variability, though serial analyses within individuals revealed consistency. Amounts of furosemide delivered into the urine after an intravenous dose correlated significantly to that after an oral dose implying that the interindividual variability is not caused primarily by variability in absorption in either group. Overall, disposition kinetics of furosemide did not differ between groups. Because of heterogeneity of renal and cardiac function among the patients, we were able to demonstrate correlations of plasma and renal clearance of furosemide with renal function; in turn, renal function correlated with left ventricular ejection fraction. Consequently, some patients had changes in furosemide disposition, but, for the most part, differences in response to furosemide were caused by abnormal responses to, rather than changed handling of the diuretic.

Absorption↗
PubMed1987

Na+, K+, and BP homeostasis in man during furosemide: effects of prazosin and captopril.

Furosemide increases sodium (Na+) and potassium (K+) excretion but if dietary salt is provided, a compensatory reduction in Na+ and K+ excretion follows which restores neutral balances within 18 to 24 hours. This compensation is not interrupted by blockade of the renin-angiotensin-aldosterone system (RAA) alone with captopril. Since plasma norepinephrine concentration increases after furosemide and alpha 1 adrenoreceptors can mediate enhanced Na+ reabsorption, we administered prazosin (2 mg 6 hr-1) to six normal volunteers consuming a daily intake of 270 mmol of Na+ and 75 mmol of K+, and added captopril (25 mg 6 hr-1) for an additional day to block the RAA system concurrently. Furosemide (40 mg day-1) was given for the last four days. Prazosin given alone before the diuretic reduced (P less than 0.05) BP and plasma angiotensin II (AII) concentration and increased body weight and heart rate. However, when given with furosemide, neither prazosin nor prazosin with captopril modified the short-term natriuretic or kaliuretic responses to furosemide, or the ensuing compensatory reductions in Na+ and K+ excretion. Accordingly, cumulative balances for Na+ and K+ remained neutral over four days of diuretic administration. Neither drug altered the renal responsiveness to the diuretic which was assessed from the relationship between renal Na+ and K+ excretion and diuretic elimination. Although the BP was maintained when furosemide was given alone, when given with prazosin and captopril, the mean BP fell by 13 +/- 5 mm Hg (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Tubular hypertrophy due to work load induced by furosemide is associated with increases of IGF-1 and IGFBP-1.

We have examined the expression of insulin-like growth factor 1 (IGF-1), IGF binding protein-1 (IGFBP-1), and IGF binding protein-3 (IGFBP-3) in the rat distal nephron during increased cell work load and hypertrophy, induced by the diuretic, furosemide. Furosemide was given for six days to increase distal sodium delivery and uptake. To mitigate salt loss, the animals drank 0.8% NaCl and 0.1% KCl. Control rats were infused with vehicle (0.9% saline) and drank tap water. Furosemide increased urinary volume (13-fold) and sodium excretion (eightfold), and decreased urine osmolarity (fourfold). By immunocytochemistry, staining for IGF-1 and IGFBP-1 was markedly increased in distal convoluted tubules and cortical collecting ducts; both segments also underwent hypertrophy. Increased staining for the peptides was evident early (1 hr, 18 hr) after furosemide, prior to hypertrophy of cells. Whereas transcripts of IGF-1 and IGFBP-3 mRNA showed little or no increase in extracts from furosemide-treated kidney cortices, IGFBP-1 mRNA was increased threefold 18 hours after furosemide. Alterations of IGF-1 and IGFBP-1 were independent of changes in plasma aldosterone, glucocorticoids or arginine vasopressin. That IGFBP-1 mRNA increased threefold without significant changes in IGF-1 mRNA suggests that hypertrophic stimuli might initially induce the synthesis of IGF binding protein followed by the trapping of extracellular IGF-1. The present study raises the possibility of IGF-1 and IGFBP-1 being involved in processes that lead to tubular hypertrophy. IGFBP-1 may regulate these effects by binding to and interaction with IGF-1.

Animals↗
PubMed2003

An orally active adenosine A1 receptor antagonist, FK838, increases renal excretion and maintains glomerular filtration rate in furosemide-resistant rats.

1. Loop and thiazide diuretics are common therapeutic agents for the treatment of sodium retention and oedema. However, resistance to diuretics and decreases in renal function can develop during diuretic therapy. Adenosine causes renal vasoconstriction, sodium reabsorption, and participates in the tubuloglomerular feedback mechanism for the regulation of glomerular filtration rate. 2. We tested the hypothesis that the selective adenosine A(1) receptor antagonist FK838 is orally active and causes diuresis and natriuresis, but maintains glomerular filtration rate in normal rats or in rats with furosemide resistance. 3. In normal male Sprague - Dawley rats, FK838 dose-dependently increased urine flow and sodium and chloride excretion while sparing potassium. In combination with furosemide, FK838 enhanced the diuretic and natriuretic actions of furosemide to the same extent as hydrochlorothiazide and did not increase the potassium loss in normal rats. In furosemide-resistant rats, FK838 increased urine flow and electrolyte excretion to a greater extent than hydrochlorothiazide. In addition, hydrochlorothiazide significantly decreased glomerular filtration rate, whereas FK838 maintained glomerular filtration rate in furosemide-resistant rats. 4. This study shows that the adenosine A(1) receptor antagonist FK838 is orally active and causes potent diuresis and natriuresis and maintains glomerular filtration rate in normal or furosemide-resistant rats. Adenosine A(1) receptor antagonists may be novel therapeutics for the treatment of oedema in normal or otherwise diuretic-resistant patients.

Adenosine A1 Receptor Antagonists↗
PubMed2002

Determination of furosemide in urine samples by direct injection in a micellar liquid chromatographic system.

A sensitive, selective and efficient micellar liquid chromatographic (MLC) procedure was developed for the determination of furosemide (4-chloro-N-furfuryl-5-sulfamoylanthranilic acid) in urine samples by direct injection and UV detection. The procedure makes use of a C18 reversed-phase column and a micellar mobile phase of 0.05 mol l(-1) sodium dodecyl sulfate-6% v/v propanol and phosphate buffer at pH 3 to resolve furosemide from its photochemical degradation products. The importance of protecting the standards and urine samples to be analysed from light in the assay of furosemide, avoiding its degradation, was verified. The limit of quantification was 0.15 microg ml(-1) and the relative standard deviation of the inter-day assay was 0.8-0.04% in the 6-82 microg ml(-1) range. Detection of urinary excretion of furosemide was followed up to 12 h after ingestion of the drug by a healthy volunteer. No potential interference from the major metabolite (furosemide acylglucuronide) and its hydrolytic product (4-chloro-5-sulfamoylanthranilic acid) was observed. Commonly administered drugs also did not interfere. The proposed MLC procedure permits the rapid and reproducible measurement of low levels of furosemide in a small amount of urine.

Chromatography, High Pressure Liquid↗
PubMed2000

Effects of furosemide on medullary oxygenation in younger and older subjects.

UNLABELLED: Renal medullary hypoxia is characteristic of mammalian kidneys and can be assessed noninvasively in animals and humans by blood oxygen level-dependent magnetic resonance imaging (BOLD MRI). Water diuresis has been shown to improve medullary oxygenation in young human subjects but not in elderly subjects, a difference attributed to a decline in renal prostaglandin production with age. Loop diuretics such as furosemide also increase medullary oxygenation in experimental animals, by inhibiting active transport and oxygen consumption in the medullary thick ascending limb. We examined, using BOLD MRI, this response to furosemide in eight younger (23 to 34 years) and eight elderly (64 to 81 years) healthy women. We also attempted to assess the role of prostaglandins in age-related differences, using ibuprofen to inhibit prostaglandin E2 synthesis. Renal medullary oxygenation, initially low, increased during furosemide diuresis in younger subjects. In the older population, however, furosemide usually elicited little or no change in oxygenation of the renal medulla, despite profuse diuresis. Ibuprofen did not inhibit the action of furosemide to improve medullary pO2 in younger subjects. CONCLUSIONS: The action of loop diuretics to improve medullary oxygenation, apparent in younger subjects, is blunted by normal aging. Inhibition of prostaglandin synthesis did not counteract the effect of furosemide in younger subjects, suggesting that a decline in prostaglandin E2 production with age is not the central cause of this age-related defect.

Adult↗
PubMed2003

Furosemide terminates limbic status epilepticus in freely moving rats.

PURPOSE: To evaluate the anticonvulsant properties of furosemide and to determine sedative side effects compared with pentobarbital and diuretic side effects compared with saline-treated controls in an experimental model of limbic status epilepticus. METHODS: Self-sustaining status epilepticus was induced in rats by continuous electrical stimulation of the perforant path. Five minutes after the end of the stimulation, animals were given 100 mg/kg furosemide, 30 mg/kg pentobarbital, or an equal amount of saline, intraperitoneally. After administration of the substance, animals were monitored clinically and electrographically for 3 h regarding status epilepticus, level of sedation, and diuresis. RESULTS: In seven of 10 animals, furosemide terminated status epilepticus after 68 +/- 26 min, whereas pentobarbital was successful in all animals after 5 +/- 0.8 min. In contrast to pentobarbital, sedation did not occur with furosemide. Weight loss after furosemide was 10.2 +/- 1.7% compared with 6.5 +/- 1.1% in animals given saline (p < 0.001). CONCLUSIONS: The results suggest that furosemide may serve as an alternative or additional agent for refractory complex partial status epilepticus in patients in whom common anesthetics are not justifiable.

Animals↗
PubMed2000

Effect of furosemide on the plasma concentration and urinary excretion of purine bases, adenosine, and uridine.

To examine whether furosemide affects the plasma concentration and urinary excretion of purine bases, adenosine, and uridine, we administered 20 mg furosemide intravenously to 6 healthy subjects. Furosemide decreased the plasma concentration of hypoxanthine by 39% and increased plasma renin activity (PRA) and the plasma concentration of protein by 3.4-fold and 9%, respectively, at 90 minutes after administration. Furthermore, it decreased the urinary excretion of hypoxanthine, xanthine, and uric acid by 47%, 49%, and 49%, respectively, and the fractional clearance of xanthine and uric acid by 44% and 47%, respectively, during the 1-hour period between 60 and 120 minutes after administration. However, furosemide did not affect the plasma concentration or urinary excretion of adenosine and uridine. In addition, in an in vitro incubation study of erythrocytes, furosemide (10 microg/mL) did not affect the concentration of hypoxanthine in the incubation medium or the activity of erythrocyte purine nucleoside phosphorylase and 5'-nucleotidase. These results imply that xanthine may share a renal transport pathway with uric acid. Further, it is suggested that the furosemide-induced decrease in hypoxanthine may be ascribable to a decrease in adenosine triphosphate (ATP) degradation related to the inhibition of chloride transport in the body.

Adenosine↗
PubMed2001

Effect of furosemide on renal excretion of oxypurinol and purine bases.

To examine whether furosemide affects the plasma concentration and urinary excretion of purine bases and oxypurinol, we administered allopurinol (300 mg) orally to 6 healthy subjects and then administered furosemide (20 mg) intravenously 10 hours later. Furosemide (20 mg) decreased the urinary excretion of uric acid by 40% (P < .01), oxypurinol by 39% (P < .05), and xanthine by 43% (P < .05) and the fractional clearance of uric acid by 45% (P < .01) and oxypurinol by 34% (P < .05) when measured 1 to 2 hours after administration. Moreover, furosemide increased the plasma concentration of uric acid by 6% at 1.5 hours after administration. These results indicate that furosemide may decrease the urinary excretion of uric acid and oxypurinol by acting on their common renal transport pathway(s). In addition, it is suggested that the effect of furosemide on oxypurinol is clinically important, since the hypouricemic effect of allopurinol may become more potent as a result.

Administration, Oral↗
PubMed2002

Is induction of fetal diuresis with intraamniotic furosemide effective for the removal of intestinal waste products from amniotic fluid?

AIM: In gastroschisis, contact with amniotic fluid (AF) causes intestinal damage. Intraamniotic meconium has been shown to be responsible for the intestinal damage, and intestinal damage has been shown to correlate with intraamniotic meconium concentrations. Intraamniotic meconium below a threshold level does not cause intestinal damage. Intraamniotic meconium concentrations can be lowered by AF exchange. Can induction of foetal diuresis by an intraamniotic injection of furosemide be used as an alternative method for the same purpose? METHOD: Pregnant rabbits on the 23rd - 25th gestational days (normal gestation time: 31 - 33 days) were divided into two groups, the control group and the furosemide group. Initial AF samples were taken, then either 5 mg/kg furosemide or a placebo was injected into the amniotic cavity. Final AF samples were obtained 6 hours later. AF urea nitrogen, creatinine, amylase, alkaline phosphatase and bilirubin levels were determined. RESULTS: There was no significant difference between the initial and final levels of AF urea nitrogen, creatinine, bilirubin, amylase, and alkaline phosphatase in the control group, while the final AF urea nitrogen and creatinine levels of the furosemide group were not significantly different from the initial levels (p > 0.05). Final AF bilirubin, amylase and alkaline phosphatase levels of the furosemide group were significantly decreased compared with initial levels (p < 0.01). CONCLUSION: Induction of foetal diuresis with intraamniotic furosemide is effective for the removal of intestinal waste products from amniotic fluid.

Amnion↗