Investigations into the mode of action of furosemide have utilized micropuncture studies in rats, stop flow experiments in dogs and various clearance studies in both humans and experimental animals. It has been demonstrated that furosemide inhibits primarily the absorption of sodium and chloride not only in the proximal and distal tubules but also in the loop of Henle. The high degree of efficacy is largely due to the unique site of action. The action on the distal tubule is independent of any inhibitory effect on carbonic anhydrase and aldosterone.
Recent evidence suggests that furosemide glucuronide is the only or at least the major biotransformation product of furosemide in man. Furosemide is extensively bound to plasma proteins, mainly to albumin. Plasma concentrations ranging from 1 to 400 mcg/mL are 91% to 99% bound in healthy individuals. The unbound fraction averages 2.3% to 4.1% at therapeutic concentrations.
The onset of diuresis following oral administration is within one hour. The peak effect occurs within the first or second hour. The duration of diuretic effect is 6 to 8 hours.
In fasted normal men, the mean bioavailability of furosemide from furosemide tablets and furosemide oral solution is 64% and 60%, respectively, of that from an intravenous injection of the drug. Although furosemide is more rapidly absorbed from the oral solution (50 minutes) than from the tablet (87 minutes), peak plasma levels and area under the plasma concentration-time curves do not differ significantly. Peak plasma concentrations increase with increasing dose but times-to-peak do not differ among doses. The terminal half-life of furosemide is approximately 2 hours.
Significantly more furosemide is excreted in urine following the IV injection than after the tablet or oral solution. There are no significant differences between the two oral formulations in the amount of unchanged drug excreted in urine.
Furosemide binding to albumin may be reduced in elderly patients. Furosemide is predominantly excreted unchanged in the urine. The renal clearance of furosemide after intravenous administration in older healthy male subjects (60 to 70 years of age) is statistically significantly smaller than in younger healthy male subjects (20 to 35 years of age). The initial diuretic effect of furosemide in older subjects is decreased relative to younger subjects.
In patients with hepatic cirrhosis and ascites, furosemide therapy is best initiated in the hospital. In hepatic coma and in states of electrolyte depletion, therapy should not be instituted until the basic condition is improved. Sudden alterations of fluid and electrolyte balance in patients with cirrhosis may precipitate hepatic coma; therefore, strict observation is necessary during the period of diuresis. Supplemental potassium chloride and, if required, an aldosterone antagonist are helpful in preventing hypokalemia and metabolic alkalosis.
If increasing azotemia and oliguria occur during treatment of severe progressive renal disease, furosemide should be discontinued.
Cases of tinnitus and reversible or irreversible hearing impairment and deafness have been reported. Reports usually indicate that furosemide ototoxicity is associated with rapid injection, severe renal impairment, the use of higher than recommended doses, hypoproteinemia or concomitant therapy with aminoglycoside antibiotics, ethacrynic acid, or other ototoxic drugs. If the physician elects to use high dose parenteral therapy, controlled intravenous infusion is advisable (for adults, an infusion rate not exceeding 4 mg furosemide per minute has been used)..
Excessive diuresis may cause dehydration and blood volume reduction with circulatory collapse and possibly vascular thrombosis and embolism, particularly in elderly patients. As with any effective diuretic, electrolyte depletion may occur during furosemide therapy, especially in patients receiving higher doses and a restricted salt intake. Hypokalemia may develop with furosemide, especially with brisk diuresis, inadequate oral electrolyte intake, when cirrhosis is present, or during concomitant use of corticosteroids, ACTH, licorice in large amounts, or prolonged use of laxatives. Digitalis therapy may exaggerate metabolic effects of hypokalemia, especially myocardial effects.
All patients receiving furosemide therapy should be observed for these signs or symptoms of fluid or electrolyte imbalance (hyponatremia, hypochloremic alkalosis, hypokalemia, hypomagnesemia or hypocalcemia): dryness of mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Increases in blood glucose and alterations in glucose tolerance tests (with abnormalities of the fasting and 2-hour postprandial sugar) have been observed, and rarely, precipitation of diabetes mellitus has been reported.
In patients with severe symptoms of urinary retention (because of bladder emptying disorders, prostatic hyperplasia, urethral narrowing), the administration of furosemide can cause acute urinary retention related to increased production and retention of urine. Thus, these patients require careful monitoring, especially during the initial stages of treatment.
In patients at high risk for radiocontrast nephropathy, furosemide can lead to a higher incidence of deterioration in renal function after receiving radiocontrast compared to high-risk patients who received only intravenous hydration prior to receiving radiocontrast.
In patients with hypoproteinemia (e.g., associated with nephrotic syndrome) the effect of furosemide may be weakened and its ototoxicity potentiated.
Asymptomatic hyperuricemia can occur and gout may rarely be precipitated.
Patients allergic to sulfonamides may also be allergic to furosemide. The possibility exists of exacerbation or activation of systemic lupus erythematosus.
As with many other drugs, patients should be observed regularly for the possible occurrence of blood dyscrasias, liver or kidney damage, or other idiosyncratic reactions.
Information for Patients
Patients receiving furosemide should be advised that they may experience symptoms from excessive fluid and/or electrolyte losses. The postural hypotension that sometimes occurs can usually be managed by getting up slowly. Potassium supplements and/or dietary measures may be needed to control or avoid hypokalemia.
Patients with diabetes mellitus should be told that furosemide may increase blood glucose levels and thereby affect urine glucose tests. The skin of some patients may be more sensitive to the effects of sunlight while taking furosemide.
Hypertensive patients should avoid medications that may increase blood pressure, including over-the-counter products for appetite suppression and cold symptoms.
Serum electrolytes (particularly potassium), CO2, creatinine and BUN should be determined frequently during the first few months of furosemide therapy and periodically thereafter. Serum and urine electrolyte determinations are particularly important when the patient is vomiting profusely or receiving parenteral fluids. Abnormalities should be corrected or the drug temporarily withdrawn. Other medications may also influence serum electrolytes.
Reversible elevations of BUN may occur and are associated with dehydration, which should be avoided, particularly in patients with renal insufficiency.
Urine and blood glucose should be checked periodically in diabetics receiving furosemide, even in those suspected of latent diabetes.
Furosemide may lower serum levels of calcium (rarely cases of tetany have been reported) and magnesium. Accordingly, serum levels of these electrolytes should be determined periodically.
In premature infants furosemide may precipitate nephrocalcinosis/nephrolithiasis, therefore renal function must be monitored and renal ultrasonography performed. (See PRECAUTIONS: Pediatric Use)
Furosemide may increase the ototoxic potential of aminoglycoside antibiotics, especially in the presence of impaired renal function. Except in life-threatening situations, avoid this combination.
Furosemide should not be used concomitantly with ethacrynic acid because of the possibility of ototoxicity. Patients receiving high doses of salicylates concomitantly with furosemide, as in rheumatic disease, may experience salicylate toxicity at lower doses because of competitive renal excretory sites.
There is a risk of ototoxic effects if cisplatin and furosemide are given concomitantly. In addition, nephrotoxicity of nephrotoxic drugs such as cisplatin may be enhanced if furosemide is not given in lower doses and with positive fluid balance when used to achieve forced diuresis during cisplatin treatment.
Furosemide has a tendency to antagonize the skeletal muscle relaxing effect of tubocurarine and may potentiate the action of succinylcholine.
Lithium generally should not be given with diuretics because they reduce lithium’s renal clearance and add a high risk of lithium toxicity.
Furosemide combined with angiotensin converting enzyme inhibitors or angiotensin II receptor blockers may lead to severe hypotension and deterioration in renal function, including renal failure. An interruption or reduction in the dosage of furosemide, angiotensin converting enzyme inhibitors, or angiotensin receptor blockers may be necessary.
Potentiation occurs with ganglionic or peripheral adrenergic blocking drugs.
Furosemide may decrease arterial responsiveness to norepinephrine. However, norepinephrine may still be used effectively.
Simultaneous administration of sucralfate and furosemide tablets may reduce the natriuretic and antihypertensive effects of furosemide. Patients receiving both drugs should be observed closely to determine if the desired diuretic and/or antihypertensive effect of furosemide is achieved. The intake of furosemide and sucralfate should be separated by at least 2 hours.
In isolated cases, intravenous administration of furosemide within 24 hours of taking chloral hydrate may lead to flushing, sweating attacks, restlessness, nausea, increase in blood pressure, and tachycardia. Use of furosemide concomitantly with chloral hydrate is therefore not recommended.
Phenytoin interferes directly with renal action of furosemide. There is evidence that treatment with phenytoin leads to decrease intestinal absorption of furosemide, and consequently to lower peak serum furosemide concentrations.
Methotrexate and other drugs that, like furosemide, undergo significant renal tubular secretion may reduce the effect of furosemide. Conversely, furosemide may decrease renal elimination of other drugs that undergo tubular secretion. High-dose treatment of both furosemide and these other drugs may result in elevated serum levels of these drugs and may potentiate their toxicity as well as the toxicity of furosemide.
Furosemide can increase the risk of cephalosporin-induced nephrotoxicity even in the setting of minor or transient renal impairment.
Concomitant use of cyclosporine and furosemide is associated with increased risk of gouty arthritis secondary to furosemide-induced hyperurecemia and cyclosporine impairment of renal urate excretion.
High doses (> 80 mg) of furosemide may inhibit the binding of thyroid hormones to carrier proteins and result in transient increase in free thyroid hormones, followed by an overall decrease in total thyroid hormone levels.
One study in six subjects demonstrated that the combination of furosemide and acetylsalicylic acid temporarily reduced creatinine clearance in patients with chronic renal insufficiency. There are case reports of patients who developed increased BUN, serum creatinine and serum potassium levels, and weight gain when furosemide was used in conjunction with NSAIDs.
Literature reports indicate that coadministration of indomethacin may reduce the natriuretic and antihypertensive effects of furosemide in some patients by inhibiting prostaglandin synthesis. Indomethacin may also affect plasma renin levels, aldosterone excretion, and renin profile evaluation. Patients receiving both indomethacin and furosemide should be observed closely to determine if the desired diuretic and/or antihypertensive effect of furosemide is achieved.
Carcinogenesis, Mutagenesis, Impairment of Fertility
Furosemide was tested for carcinogenicity by oral administration in one strain of mice and one strain of rats. A small but significantly increased incidence of mammary gland carcinomas occurred in female mice at a dose 17.5 times the maximum human dose of 600 mg. There were marginal increases in uncommon tumors in male rats at a dose of 15 mg/kg (slightly greater than the maximum human dose) but not at 30 mg/kg.
Furosemide was devoid of mutagenic activity in various strains of Salmonella typhimurium when tested in the presence or absence of an in vitro metabolic activation system, and questionably positive for gene mutation in mouse lymphoma cells in the presence of rat liver S9 at the highest dose tested. Furosemide did not induce sister chromatid exchange in human cells in vitro, but other studies on chromosomal aberrations in human cells in vitro gave conflicting results. In Chinese hamster cells it induced chromosomal damage but was questionably positive for sister chromatid exchange. Studies on the induction by furosemide of chromosomal aberrations in mice were inconclusive. The urine of rats treated with this drug did not induce gene conversion in Saccharomyces cerevisiae.
Furosemide produced no impairment of fertility in male or female rats at 100 mg/kg/day (the maximum effective diuretic dose in the rat and 8 times the maximal human dose of 600 mg/day).
Teratogenic Effects. Pregnancy Category C
Furosemide has been shown to cause unexplained maternal deaths and abortions in rabbits at 2, 4 and 8 times the maximal recommended human dose. There are no adequate and well-controlled studies in pregnant women. Furosemide should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Treatment during pregnancy requires monitoring of fetal growth because of the potential for higher birth weights.
The effects of furosemide on embryonic and fetal development and on pregnant dams were studied in mice, rats and rabbits.
Furosemide caused unexplained maternal deaths and abortions in the rabbit at the lowest dose of 25 mg/kg (two times the maximal recommended human dose of 600 mg/day). In another study, a dose of 50 mg/kg (four times the maximal recommended human dose of 600 mg/day) also caused maternal deaths and abortions when administered to rabbits between Days 12 and 17 of gestation. In a third study, none of the pregnant rabbits survived a dose of 100 mg/kg. Data from the above studies indicate fetal lethality that can precede maternal deaths.
The results of the mouse study and one of the three rabbit studies also showed an increased incidence and severity of hydronephrosis (distention of the renal pelvis and, in some cases, of the ureters) in fetuses derived from the treated dams as compared with the incidence in fetuses from the control group.
Because it appears in breast milk, caution should be exercised when furosemide is administered to a nursing mother.
Furosemide may inhibit lactation.
In premature infants, furosemide may precipitate nephrocalcinosis/nephrolithiasis. Nephrocalcinosis/nephrolithiasis has also been observed in children under 4 years of age with no history of prematurity who have been treated chronically with furosemide. Monitor renal function, and renal ultrasonography should be considered, in pediatric patients receiving furosemide.
If furosemide is administered to premature infants during the first weeks of life, it may increase the risk of persistence of patent ductus arteriosus.
Controlled clinical studies of furosemide did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for the elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal or cardiac function, and of concomitant disease or other drug therapy.
This drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection and it may be useful to monitor renal function.
The principal signs and symptoms of overdosage with furosemide are dehydration, blood volume reduction, hypotension, electrolyte imbalance, hypokalemia and hypochloremic alkalosis, and are extensions of its diuretic action.
The acute toxicity of furosemide has been determined in mice, rats and dogs. In all three, the oral LD50 exceeded 1000 mg/kg body weight, while the intravenous LD50 ranged from 300 to 680 mg/kg. The acute intragastric toxicity in neonatal rats is 7 to 10 times that of adult rats.
The concentration of furosemide in biological fluids associated with toxicity or death is not known.
Treatment of overdosage is supportive and consists of replacement of excessive fluid and electrolyte losses. Serum electrolytes, carbon dioxide level and blood pressure should be determined frequently. Adequate drainage must be assured in patients with urinary bladder outlet obstruction (such as prostatic hypertrophy).
Hemodialysis does not accelerate furosemide elimination.
Furosemide Tablets, USP are available as tablets for oral administration. Each tablet for oral administration contains 20 mg, 40 mg or 80 mg of furosemide, USP.
The 20 mg tablets are white, round, unscored tablets debossed with M2. They are available as follows:
bottles of 100 tablets
bottles of 1000 tablets
The 40 mg tablets are white, round, scored tablets debossed with MYLAN over 216 on one side and the tablet and 40 on the other side. They are available as follows:
bottles of 100 tablets
bottles of 1000 tablets
The 80 mg tablets are white, round, scored tablets debossed with MYLAN over 232 on one side of the tablet and 80 on the other side. They are available as follows:
bottles of 100 tablets
bottles of 500 tablets
Store at 20° to 25°C (68° to 77°F). [See USP Controlled Room Temperature.]
Protect from light.
Dispense in a tight, light-resistant container as defined in the USP using a child-resistant closure. Exposure to light may cause a slight discoloration. Discolored tablets should not be dispensed.
Mylan Pharmaceuticals Inc.
Morgantown, WV 26505 U.S.A.
REVISED APRIL 2016
NADA 129-034, Approved by FDA
Furosemide is not USP for dissolution.
For use in dogs only
Federal law restricts this drug to use by or on the order of a licensed veterinarian.
Furosemide is a potent loop diuretic which is a derivative of anthranilic acid. The structure is:
Chemical Name: 4-Chloro-N-furfuryl-5-sulfamoylanthranilic acid.
Furosemide is pharmacodynamically characterized by the following:
1) It is administered orally. It is easily absorbed from the intestinal tract and begins to act in 30 to 60 minutes after oral administration.1, 2
2) Is a loop diuretic which inhibits reabsorption of sodium and chloride at the ascending loop of Henle in the kidneys, enhancing water excretion. 3
3) A dose-response relationship and a ratio of minimum to maximum effective dose range greater than tenfold. 1
4) A high degree of efficacy, low inherent toxicity and a high therapeutic index.
The therapeutic efficacy of Furosemide Tablets is from the activity of the intact and unaltered molecule throughout the nephron, inhibiting the reabsorption of sodium not only in the proximal and distal tubule but also in the ascending limb of the loop of Henle. The prompt onset of action is a result of the drug's rapid absorption and a poor lipid solubility. The low lipid solubility and a rapid renal excretion minimize the possibility of its accumulation in tissues and organs or crystalluria. Furosemide Tablets have no inhibitory effect on carbonic anhydrase or aldosterone activity in the distal tubule. The drug possesses diuretic activity either in the presence of acidosis or alkalosis.1, 2, 4, 5, 6
Dogs - Furosemide Tablets are indicated for the treatment of edema (pulmonary congestion, ascites) associated with cardiac insufficiency and acute non-inflammatory tissue edema. In cases of edema involving cardiac insufficiency, the continued use of heart stimulants such as digitalis or its glycosides is indicated. The rationale for efficacious use of diuretic therapy is determined by the clinical pathology producing the edema.
Dosage and Administration:
The usual oral dosage of Furosemide Tablets is 1 to 2 mg/lb body weight (approximately 2.5 to 5 mg/kg). A prompt diuresis usually ensues from the initial treatment.
Administer orally once or twice daily at 6 to 8 hour intervals. The dosage should be adjusted to the individual's response. In severe edematous or refractory cases, the dose may be doubled or increased by increments of 1.0 mg per pound of body weight. The established effective dose should be administered once or twice daily. The daily schedule of administration can be timed to control the period of micturition for the convenience of the client or veterinarian. Mobilization of the edema may be most efficiently and safely accomplished by utilizing an intermittent daily dose schedule, i.e., every other day or 2 to 4 consecutive days weekly.
Diuretic therapy should be discontinued after reduction of the edema, or maintained after determining a carefully programmed dosage schedule to prevent recurrence of edema. For long-term treatment, the dose can generally be lowered after the edema has once been reduced. Re-examination and consultations with the client will enhance the establishment of a satisfactorily programmed dosage schedule. Clinical examination and serum BUN, CO2 and electrolyte determinations should be performed during the early period of therapy and periodically thereafter, especially in refractory cases. Abnormalities should be corrected or the drug temporarily withdrawn.
Dog: One-half to one 50 mg scored tablet per 25 pounds body weight. One 12.5 mg scored tablet per 5 to 10 pounds body weight.
Administer once or twice daily, permitting a 6- to 8-hour interval between treatments. In refractory or severe edematous cases, the dosage may be doubled or increased by increments of 1 mg per pound body weight as recommended in preceding paragraphs, "Dosage and Administration".
Animal reproductive studies have shown that furosemide may cause fetal abnormality and the drug is contraindicated in pregnant animals. Furosemide is contraindicated in anuria, furosemide hypersensitivity, hepatic coma, or during electrolytic imbalances. Monitor serum electrolytes, BUN and CO2 frequently. Monitor serum potassium levels and watch for signs of hypocalcemia.
Corticosteroids cause an additive potassium-depletion effect.
Furosemide Tablets are a highly effective diuretic and, if given in excessive amounts, as with any diuretic, may lead to excessive diuresis which could result in electrolyte imbalance, dehydration and reduction of plasma volume, enhancing the risk of circulatory collapse, thrombosis and embolism. Therefore, the animal should be observed for early signs of fluid depletion with electrolyte imbalance, and corrective measures administered. Excessive loss of potassium in patients receiving digitalis or its glycosides may precipitate digitalis toxicity. Caution should be exercised in animals administered potassium-depleting steroids. Correct potassium deficiency with proper dietary supplementation. If animal needs potassium supplements, use oral liquid form, do not use enteric-coated potassium tablets.
The concurrent use of furosemide with some antibiotics may be inadvisable. There is evidence that the drug enhances the nephrotoxic potential of aminoglycosides, cephalosporins and polymyxins and increases the ototoxic effects of all aminoglycosides.
Sulfonamide diuretics have been reported to decrease arterial responsiveness to pressor amines and to enhance the effect of tubocurarine. Caution should be exercised in administering curare or its derivatives to patients undergoing therapy with Furosemide Tablets and it is advisable to discontinue Furosemide Tablets for one day prior to any elective surgery.
Furosemide Tablets are a highly effective diuretic-saluretic which, if given in excessive amounts, may result in dehydration and electrolyte imbalance. Therefore, the dosage and schedule may have to be adjusted to the patient's need. The animal should be observed for early signs of electrolyte imbalance, and corrective measures administered. Early signs of electrolyte imbalance are increased thirst, lethargy, drowsiness or restlessness, fatigue, oliguria, gastro-intestinal disturbances and tachycardia. Special attention should be given to potassium levels. Furosemide Tablets may lower serum calcium levels and cause tetany in rare cases of animals having an existing hypocalcemic tendency. 7, 8, 9, 10, 11
Furosemide Tablets are contraindicated in anuria. Therapy should be discontinued in cases of progressive renal disease if increasing azotemia and oliguria occur during the treatment. Sudden alterations of fluid and electrolyte imbalance in an animal with cirrhosis may precipitate hepatic coma, therefore, observation during period of therapy is necessary. In hepatic coma and in states of electrolyte depletion, therapy should not be instituted until the basic condition is improved or corrected. Potassium supplementation may be necessary in cases routinely treated with potassium-depleting steroids.
Active or latent diabetes may on rare occasions be exacerbated by furosemide. Transient loss of auditory capacity has been experimentally produced in cats following intravenous injections of excessive doses of furosemide at a very rapid rate. 12, 13, 14
Furosemide demonstrates a very low order of either acute or chronic toxicity. The drug is rapidly absorbed and excreted by both glomerular filtration and tubular secretion. The rates of excretion are of such magnitude that cumulation of furosemide does not occur despite repeated administrations. 15
The main effect observed in clinical toxicity is an abnormality of fluid and electrolyte imbalances. Ototoxicity resulting in transient loss of hearing has been reported with furosemide. 15
A safety study was performed in dogs to determine the effects of Furosemide Tablets at increasing dosages and time elements. The dosage levels were 2 mg/lb body weight (upper recommended dosage), 6 mg/lb body weight (3X upper recommended dosage) and 10 mg/lb body weight (5X upper recommended dosage). The treatment period ranged up to nine days in length. Results demonstrate a mild dehydration at the 5X level with a slight elevation of hemoglobin and hematocrit levels. Serum levels of potassium and chloride were slightly lowered in the higher dosage groups. Cumulative evaluation of the data demonstrates that Furosemide Tablets are safe when administered at the upper level of the recommended dosage for a duration of nine consecutive days.
To report suspected adverse reactions, to obtain a Material Safety Data Sheet or for technical assistance, call 1-866-638-2226.
Store at 20° to 25°C (68° to 77°F), excursions permitted between 15° and 30°C (between 59° and 86°F).
Furosemide Tablets are available in 12.5 mg and 50 mg strength and supplied in bottles containing 500 tablets.
NDC 13985-586-12 - 12.5 mg – 500 tablets
NDC 13985-585-50 - 50 mg – 500 tablets
- Timmerman, R.J., F.R. Springman and R.K. Thoms, 1964. Evaluation of Furosemide, a New Diuretic Agent. Current Therapeutic Research, 6(2): 88-94.
- Martindale, The Extra Pharmacopoeia. 27th ed. June 1977, The Pharmaceutical Press, London, 556.
- Suki, W., F.C. Rector, Jr. and D.W. Seldin, 1965. The Site of Action of Furosemide and Other Sulfonamide Diuretics in the Dog. Journal of Clinical Investigation, 44(9):1458-1469.
- Berman, L.B. and A. Ebrahimi. February 1965. Experiences with Furosemide in Renal Disease. Proceedings in the Society for Experimental Biology and Medicine, 118:333-336.
- Schmidt, H.A.E. Animal Experiments with S35 Tagged Lasix® in Canine and Ovine. Radio-chemical Pharmacological Laboratory, Farbwerke Hoechst, Frankfurt, West Germany.
- Haussler, A. and P. Hajdu. Methods Biological Identification and Results of Studies on Absorption, Elimination and Metabolism. Research Laboratories, Farbwerke Hoechst, Frankfurt, West Germany.
- Antoniou, L.D., G.M. Eisner, L.M. Slotkoff and L.S. Lilienfield. December 1967. Sodium and Calcium Transport in the Kidney. Clinical Research, 15(4):476.
- Duarte, C.G. April 1967. Effects of Furosemide (F) and Ethacrynic Acid (ETA) on the Renal Clearance of Phosphate (Cp), Ultrafilterable Calcium (CUfCa) and Magnesium (CUfMg). Clinical Research, 15(2):357.
- Duarte, C.G. October 1968. Effects of Ethacrynic Acid and Furosemide on Urinary Calcium, Phosphate and Magnesium. Metabolism, 17:867-876.
- Nielsen, S.P., O. Andersen and K.E. Steven, 1969. Magnesium and Calcium Metabolism during Prolonged Furosemide (Lasix®) Administration to Normal Rats. Acta Pharmacol, et. Toxicol., 27:469-479.
- Reimold, E.W. July 1972. The Effect of Furosemide on Hypercalcemia Due to Dihydrotachysterol, Metabolism, 21(7).
- Brown, R.D. and T.W. McElwee, Jr. Effects of Intra-Arterially and Intravenously Administered Ethacrynic Acid and Furosemide on Cochlear N1 in Cats. Toxicology and Applied Pharmacology, 22:589-594, 1972.
- Mathog, R.H., W.G. Thomas and W.R. Hudson: Ototoxicity of New and Potent Diuretics. Archives of Otolaryngology, 92(1):7-13, July 1970.
- Mathog, R.H. and G.J. Matz: Ototoxic Effects of Ethacrynic Acid. Annals of Otolaryngology, Vol. 81, 1972.
- Gilman, A.G., L.S. Goodman and A. Gilman, 1980. The Pharmacological Basis of Therapeutics, Sixth ed., MacMillan Publishing Co., Inc., New York, NY, 903-907.
673835-00 / 673935-01
81821771, R.0 / 81821798, R.1
Rev. 10/2013 / Rev. 02/14
Distributed by: MWI, Boise, ID 83705 (888) 694-8381