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PubMed1982

Renal calcifications: a complication of long-term furosemide therapy in preterm infants.

During the last four years ten premature infants developed renal calcifications while receiving long-term furosemide therapy. The drug was used in infants with present ductus arteriosus and later in the same infants with chronic lung disease. They had received furosemide in a dose of at least 2 mg/kg/day for at least 12 days before calcifications were noted on abdominal roentgenograms. Calcifications included small flecks, isolated stones, staghorn calculi, and nephrocalcinosis. Analysis of stones received from our infants showed calcium oxalate and calcium phosphate. Infants who were not receiving furosemide had no calcifications. The infants with renal calcifications had rates of calcium excretion ten to 20 times that of normal, age-matched premature infants in our nursery. When chlorothiazide was given to the infants, in addition to furosemide, a four- to 15-fold decrease in calcium excretion and a radiologic dissolution of the renal calcifications were documented. It is concluded that furosemide, in doses of at least 2 mg/kg/day for at least 12 days can be associated with renal calcifications. The probable mechanism of the stone formation is hypercalciuria, primarily caused by furosemide.

Ductus Arteriosus, Patent↗
PubMed1982

Effect of furosemide on canine inferior mesenteric blood flow.

The administration of diuretics to patients receiving cardiac glycosides has been reported to be a contributing factor in the incidence of nonocclusive mesenteric infarction. Presumably, the loss of fluid induced by the diuretics results in a decrease in blood flow to the intestines. This, combined with the vasoconstrictor action of the glycosides, can result in too great a decrease in blood flow and hence the development of an infarct. The ability of diuretics to alter intestinal circulation is supported by animal studies which have shown that blood flow in the superior mesenteric artery is decreased after the administration of furosemide. Since intestinal blood flow is also, in part, supplied by the inferior mesenteric artery, it was of interest to determine the effect of the administration of furosemide on blood flow in this vessel. Following intravenous administration of furosemide (2 mg/kg), inferior mesenteric flow was found to be decreased significantly at 10 minutes and it continued to decline until approximately 40 minutes after administration of the diuretic. Blood pressure was elevated slightly (less than 10 mm Hg) for the first 30 minutes after the administration of furosemide. It would seem likely that the reduction in inferior mesenteric blood flow following administration of furosemide is probably caused by the same factors which mediate the furosemide-induced decrease in superior mesenteric blood flow.

Animals↗
PubMedDate not supplied

Furosemide effect on gastric basal secretion during exercise and postexercise restitution in healthy subjects.

The purpose of this work was determination of furosemide effect on basal gastric secretion during exercise and postexercise restitution in 8 healthy men aged 22-25 years. The investigations were performed three times determining each time the basal acid output during three successive hours. In the first test the determinations were done during one hour rest, then after intravenous furosemide administration 2 mg/kg, and again between 60 and 120 minutes after the injection. In the second test BAO was determined at rest, during one-hour exercise, and during restitution. In the third test the determinations were done at rest, during exercise preceded by furosemide injection as in the first test, and during one hour of post-exercise restitution. The exercise on a Monark cycle ergometer was, on the average, 275 210 +/- 12 500 J in the second test and 284 870 +/- 14 480 J in the third test. Furosemide caused a statistically significant decrease of BAO at rest (p less than 0.02) and during exercise (p less than 0.01), this was due to a significant reduction in gastric juice volume (p less than 0.001) and in the second hour of furosemide action also to a decrease of HCI concentration (p less than 0.05). Decreased excretion of electrolytes by the gastric mucosa was proportional to changes in gastric juice volume. The 24-hour urinary excretion of sodium, potassium and chlorides increased after furosemide in the first test (p less than 0.001), and in the third test (p less than 0.02).

Adult↗
PubMed1981

Disposition of furosemide in functionally hepatectomized dogs.

To assess the role of the liver in the elimination of furosemide, the disposition kinetics of the diuretic after intravenous administration were studied in dogs with total devascularization of the liver and sham-operated animals. Functional hepatectomy caused no significant changes in either the renal or the nonrenal clearances of furosemide; renal = 124.2 +/- 27.1 (mean +/- SE) and 106.6 +/- 17.5 ml/min and nonrenal = 148.2 +/- 11.4 and 112.6 +/- 21.0 ml/min in sham-operated and hepatectomized dogs, respectively. Devascularization of the liver had no effect on the plasma binding of furosemide which was 90.0% in the sham-operated and 88.2% in the hepatectomized animals. The steady-state volume of distribution of furosemide was relatively small, 0.70 +/- 0.09 liters/kg in control dogs and hepatectomy resulted in a reduction in this volume (0.58 +/- 0.09 liters/kg). This indicates that the liver is a significant organ for distribution of furosemide in the dog. Urinary recoveries of parent drug (43.2% of the dose in sham-operated dogs ad 49.1% in hepatectomized animals) and of its glucuronide (4.3% in sham-operated and 5.5% in hepatectomized dogs) were not influenced by hepatic devascularization. These findings demonstrate that, although nonrenal clearance accounts for about 50% of the elimination of furosemide, the liver does not play a significant role in this process in the dog.

Animals↗
PubMed1981

Effect of intravenous furosemide on serum theophylline concentration.

The effect of furosemide on the serum theophylline concentration (STC) was investigated in 10 patients at steady state on a continuous i.v. aminophylline infusion. A baseline STC was obtained 48 hours after the initiation of the maintenance infusion. The patients were monitored closely for the last 24 hours of the maintenance period with hourly flow records to assure the same continuous rate. Urine output was measured over four hours, then, a 40-mg dose of furosemide was administered i.v. over two minutes, and the aminophylline infusion was continued at the same rate. Urine output was measured for four hours after the furosemide dose, and then a second STC was obtained. The 40-mg furosemide i.v. bolus injection caused an average increase of 2.9 micrograms/ml in STC, with a range of 0.5--5.5 micrograms/ml. The urine volumes increased by an average of 995 ml above the baseline, with a range of 630--1377 ml. Both of the increases were significant at the p less than 0.005 level. Patients stabilized on a theophylline dosage regimen should be monitored closely during the addition or discontinuation of furosemide therapy. Furosemide has been shown to be another factor that can alter STC.U

Adult↗
PubMed1981

Maintenance diet and the effects of furosemide on hamsters.

Experiment 1 indicated that furosemide, a diuretic, was ineffective in causing hamsters to excrete more urinary sodium when they were fed a sodium-replete diet. Neither the experimental nor the control animals showed any appreciable change in urinary sodium concentration when injected while maintained on Purina lab chow. However, experimental animals that were fed a sodium-deficient diet and then were injected with furosemide showed an increase in urinary volume as well as in sodium concentration in comparison with controls. Experiment 2 assessed the effect of furosemide on the hamsters' intake of saline when they were presented with either 0.9% NaCl and water or 2.0% NaCl solution and water. The results indicated that this diuretic increased the animals' intake of 0.9% saline but not of 2.0% NaCl. Ten days after this experiment, the same hamsters were then tested in a situation where they were presented with both 0.9% and 2.0% saline (Experiment 3). When these animals were injected with furosemide, both groups showed increased intake of 2.0% saline but not of 0.9% NaCl. These results indicate that the outcome of two-bottle preference tests is influenced by the combinations upon which the hamster is making the paired comparison. Experiment 4 involved the comparison of the single-stimulus and double-stimulus methods in assessing the effects of furosemide injections on the saline intake of different groups of hamsters. In general, the double-stimulus method appears to be more sensitive in detecting the natriorexigenic effects of furosemide.

Animals↗
PubMed1994

[Body fluid withdrawal with isolated ultrafiltration effects persistent improvement of functional capacity in patients with chronic congestive heart failure. Furosemide does not produce the same result].

In moderate congestive heart failure pulmonary overhydration may be detected at chest X-ray even if therapy is optimized to keep the urinary output normal and to prevent weight gain and dependent edema formation. Removal of overhydration of the lung may help to define its significance. This study was aimed at investigating whether a subclinical accumulation of fluid in the lung interstitium in moderate congestive heart failure interferes with the patient's functional capacity, and whether furosemide is able to promote reabsorption of the excessive fluid. Patients whose digoxin, oral furosemide and ACE-inhibitor therapeutic regimen was kept constant, were randomly allocated to ultrafiltration (8 cases) or iv bolus (mean dose = 248 mg) of supplemental furosemide (8 cases). The amount of body fluid removed with each method approximated 1.600 ml. Functional performance was assessed with cardiopulmonary exercise tests. Soon after fluid withdrawal with either procedure the filling pressures of the two ventricles and body weight were reduced and plasma renin activity, norepinephrine and aldosterone were augmented. After furosemide hormones remained elevated in the subsequent 4 days, and, during this period, patients had positive water metabolism, recovery of the elevated ventricular filling pressures, recurrence of lung congestion without any improvement in functional capacity. In ultrafiltrated patients, renin, norepinephrine and aldosterone fell below control values within the first 48 hours and water metabolism was equilibrated at a new set point (less fluid intake and diuresis without weight gain). Functional capacity in these patients was improved through favorable circulatory and ventilatory adjustments consequent on reabsorption of lung water. This may also have restored the ability of the lung to clear norepinephrine, thus restraining its facilitation of renin release. Improvement persisted at 3 months after the procedure. In congestive heart failure the set point of fluid balance is altered despite oral furosemide; supplemental iv furosemide does not shift the set point, at least in the presence of ACE-inhibition; excessive, although silent, lung water limits the functional capacity of the patient.

Aged↗
PubMed1995

Metabolic effects of anti-hypertensive treatment with nifedipine or furosemide: a double-blind, cross-over study.

To evaluate the metabolic effects of two anti-hypertensive agents with different actions, nifedipine 20 mg twice daily and furosemide 60 mg twice daily, 23 patients with untreated essential hypertension performed a double-blind, cross-over study in treatment periods of 5 months. Metabolic effects were evaluated by serum lipoprotein determinations, the intravenous glucose tolerance test and the hyperinsulinaemic euglycaemic clamp technique. Nifedipine and furosemide reduced blood pressure to the same extent (-14 to -15 mm Hg for supine SBP and -9 to -10 mm Hg for supine DBP, both P < 0.0001). Whereas both drugs significantly increased the levels of glycolysated haemoglobin (HbA1c, +0.24%, P < 0.005 for nifedipine and +0.43%, P < 0.001 for furosemide), only furosemide increased fasting blood glucose (+0.3 mmol/L, P < 0.01) and fasting insulin (+2.2 mU/L, P < 0.05) but impaired the early insulin response to i.v. glucose (-15 mU/L, P < 0.05). Insulin sensitivity on the other hand was significantly impaired by nifedipine treatment only (-1.6 mg/kg/min, P < 0.01). Whereas treatment with nifedipine did not change serum lipids, furosemide caused an increase in serum cholesterol (+0.2 mmol/L, P < 0.05) because of a rise in the LDL fraction (+0.32 mmol/L, P < 0.001). The insignificant change in heart rate induced by nifedipine treatment correlated with the change in HbA1c (r = 0.50, P = 0.05) and was inversely related to the change in insulin sensitivity (r = -0.56, P < 0.05). In conclusion, both furosemide and nifedipine caused abnormalities in glucose metabolism. In the nifedipine group the effects on glucose metabolism were related to the occurrence of tachycardia suggesting that sympathetic nerve activation could be involved in the metabolic impairments.

Aged↗
PubMedDate not supplied

[Effect of furosemide on renal magnesium and calcium excretion of different ages (II)].

Thirty normal students, including senior high, junior high and elementary school, were the subject for furosemide test. Ten cases, in each age group, were given oral furosemide 2 mg/kg for three consecutive days. The result showed there were increasing urinary magnesium and calcium excretion among the three different age groups after oral furosemide (P < 0.05). Successive increase of urinary magnesium and calcium excretion of senior high school students is more obvious than those of junior high and elementary school students. It is suggested that there is more effective action on renal magnesium and calcium excretion for senior high school students after oral furosemide than that for the junior high and elementary school students. It is obvious that increasing dosage of furosemide would induce more calcium excretion than magnesium excretion among students of the three age groups. Therefore, it encouraged to drink the proper amount of water to decrease the incidence of hypercalciuric stone when furosemide should be used.

Adolescent↗
PubMedDate not supplied

[Levels of plasma proteins in patients with ene stage renal failure treated with peritoneal dialysis with an addition of furosemide to dialysis fluid].

This study aimed at evaluating an effect of repeated intraperitoneal furosemide administration on plasma proteins in patients with uremia given the drug to increase intermittent peritoneal dialysis efficiency. Patients (n = 6) dialysed for 48-60 hours per week furosemide was added to dialysis fluid in the dose of 1.2-2.0 g per 1 dialysis weekly for 3 months. A control group consisted of patients (n = 6) dialysed without furosemide. Plasma total proteins, albumin, total globulins, IgG, and IgA were determined in all patients. At the same time, plasma furosemide levels were monitored. A 3-month treatment with dialyses supplemented with furosemide decreased plasma protein levels especially IgG (p < 0.5) in comparison with dialyses without the drug. Furosemide plasma levels remained below ototoxic levels (over 50 micrograms/mL) during the treatment.

Adult↗
PubMed1977

Metabolic clearance of furosemide in the rat.

The effect of probenecid on the metabolic clerance of [35S]furosemide was examined in Sprague-Dawley rats by the single injection technique. Metabolic clearance was found to decrease from 1.74+/-0.11 ml/min in animals which received furosemide alone to 1.06+/-0.10 ml/min in animals which received both furosemide and probenecid. Estimation of urine and biliary clearance revealed that approximately two-thirds of the metabolic clearance was due to urinary clearance and one-third to biliary clearance, and that both decreased after probenecid administration. Thin-layer chromatographic studies indicated furosemide was metabolized by both liver and kidney but also secreted in unchanged form in urine, and that the proportion of unaltered furosemide to metabolite in urine was increased by probenecid. Further studies indicated that phenobarbital pretreatment had no effect on either hepatic or renal clearance of furosemide and that bile clearance was not altered by acute bilateral nephrectomy.

Animals↗
PubMed1996

Effects of furosemide on hemorheologic alterations induced by incremental treadmill exercise in thoroughbreds.

OBJECTIVE: To determine whether furosemide treatment altered the blood flow properties and serum and RBC electrolyte concentrations of Thoroughbreds during submaximal treadmill exercise. DESIGN: Thoroughbreds were subjected to submaximal treadmill exercise with and without treatment with furosemide (1 mg/kg of body weight, IV). ANIMALS: 5 healthy Throughbreds that had raced within the past year and had no history of exercise-induced pulmonary hemorrhage. PROCEDURE: Venous blood samples were obtained before exercise, at treadmill speeds of 9 and 13 m/s, and 10 minutes after exercise, and hemorheologic and electrolyte test results were determined. RESULTS: Hemorheologic changes 60 minutes after furosemide administration included increased PCV, plasma total protein concentration, whole blood viscosity, mean RBC volume, and RBC potassium concentration, and decreased serum potassium concentration, serum chloride concentration, and RBC chloride concentration. Furosemide treatment attenuated the exercise-associated changes in RBC size, serum sodium concentration, serum potassium concentration, RBC potassium and chloride concentrations, and RBC density; exacerbated exercise-associated increases in whole blood viscosity; and had no effect on RBC filterability. CONCLUSIONS: The hemorheologic effects of furosemide probably occurred secondary to total body and transmembrane fluid and electrolyte fluxes and would not improve blood flow properties. CLINICAL RELEVANCE: The beneficial effects of furosemide treatment in reducing the severity of bleeding in horses with exercise-induced pulmonary hemorrhage cannot be explained by improved blood flow properties.

Animals↗
PubMed1996

Bromobenzene and furosemide hepatotoxicity: alterations in glutathione, protein thiols, and calcium.

The nature of the events whereby the reactive intermediates resulting from the bioactivation of bromobenzene and furosemide induce hepatotoxicity is unknown. To examine a role for disturbances in intracellular calcium homeostasis, secondary to a depletion in cellular reduced glutathione (GSH) and reduced protein thiols (PSHs), isolated mouse hepatocytes were exposed to cytotoxic concentrations of bromobenzene or furosemide. Cytosolic calcium concentration, as well as thiol status, was determined. The incubation of hepatocytes with 3.0 mM bromobenzene, and subsequent additions (1.2 mM) of the agent every hour, resulted in significant GSH depletion. The loss of plasma membrane integrity at 1.5 h preceded both a rise in the cytosolic Ca2+ concentration and depletion of total PSH content. Furosemide (1.0 mM) produced a 70% depletion in cellular GSH content in isolated hepatocytes. The initiation of cell damage occurred concurrently with both a rise in the cytosolic Ca2+ concentration and a depletion of total PSH content 4 h following furosemide addition. Since the increase in cytosolic Ca2+ did not precede cytotoxicity, these results do not support an initiating role for Ca2+ deregulation in bromobenzene and furosemide hepatotoxicities. In addition, depletion of PSH content did not correlate with bromobenzene- or furosemide-induced cytotoxicity.

Animals↗
PubMed1977

Effects and interactions of furosemide and acetazolamide on tubular function in rat kidney.

Furosemide and acetazolamide effects on tubular function in rat kidney have been studied by micropuncture. Furosemide produced a marked rise in fractional proximal fluid reabsorption when urine loss was not replaced, and sodium excretion rose significantly indicating a distal effect. If urinary losses were replaced proximal fractional reabsorption was depressed and fractional sodium excretion increased more than 60%. After replacing urinary losses, acetazolamide had a greater depressive effect on proximal tubular fluid reabsorption than furosemide but sodium excretion values were about 1/3 of those obtained with furosemide. Superimposition of one drug during the action of the other resulted in potentiation of proximal inhibition, suggesting a different mechanism of action. The changes observed in potassium excretion are of great interest. Separately, furosemide or acetazolamide produced kaliuresis. When furosemide was administered during acetazolamide diuresis, however, potassium excretion was reduced despite the sharp rise in sodium excretion.

Acetazolamide↗
PubMed1996

Effect of a hepatoprotective agent, YH-439, on the pharmacokinetics of furosemide and azosemide in rats.

The effect of YH-439 pretreatment on the pharmacokinetics of furosemide and azosemide was investigated after intravenous (iv) administration of furosemide, 6 mg per whole body weight, and azosemide, 10 mg per kg body weight, to rats pretreated with 3 consecutive daily oral administration of YH-439, 200 mg per kg body weight. The nonrenal clearance of furosemide (2.20 versus 3.53 ml/min/kg) increased significantly, and the 24 h-urinary excretion of furosemide (both the amount and percentages of iv dose) decreased significantly in the YH-439 treated rats when compared with those in the control rats. The results were unexpected since the metabolism of furosemide increased by pretreatment with phenobarbital (CYP2B inducer) and YH-439 pretreatment failed to affect CYP2B expression. The increased metabolism of furosemide by pretreatment with YH-439 could be due to other enzyme(s) induced by pretreatment with YH-439. Pharmacokinetic parameters of azosemide were not significantly different between the two groups of rats except t(1/2), MRT, and V(ss). The results were unexpected since azosemide metabolism increased with 3-methylchloranthane (3-MC, CYP1A inducer) and YH-439 pretreatment increased CYP1A expression. Above data indicate that the expression of CYP1A by treatment with YH-439 was not considerable when compared with that with 3-MC.

Animals↗
PubMed1997

Effects of renal papillary-medullary lesion on the antihypertensive effect of furosemide and development of salt-sensitive hypertension in Dahl-S rats.

To test the hypothesis that the long-term antihypertensive action of furosemide is mediated by a renomedullary vasodepressor substance, we measured mean arterial pressure (MAP) by radiotelemetry in Dahl-S rats with either intact or bromoethylamine-induced (BEA, 100 mg/kg i.p.) lesion of the renal papilla and medulla. Seven days of recovery after BEA administration, the rats diet was changed from 1 to 4% NaCl, and during days 8 to 31, rats were randomized to daily treatment with placebo or furosemide (50 mg/kg p.o.). Then furosemide treatment was stopped and the rat food was changed to 1% NaCl diet. After a 10-day wash-out period, renal function was measured. BEA produced a rapid (within min) and sustained increase in MAP which was accelerated during 4% NaCl diet. Furosemide prevented 4% NaCl-induced hypertension in both rats with intact kidneys and in rats with BEA-induced renal papillary-medullary lesion. A significant decrease in renal plasma flow (-34%) and glomerular filtration rate (-40%) was observed in all BEA-treated rats independent of previous furosemide treatment. In response to an i.v. load of isotonic saline (10% body weight), rats with renal papillary-medullary lesion had an impaired ability to excrete sodium. Histological examination showed that BEA-treated rats had severe lesions of the renal papilla and medulla, with light-to-moderate changes in the renal cortex. It is concluded that the antihypertensive effect of furosemide is not mediated by a renomedullary vasodepressor substance. The accelerated NaCI-sensitive hypertension in rats with BEA-induced renal papillary-medullary lesion is related to an impaired ability to excrete excess NaCl.

Animals↗
PubMed1996

Comparison of diuretic effects of glycerol with furosemide after transurethral prostatectomy.

BACKGROUND: Diuretic therapy after transurethral prostatectomy (TURP) is primarily intended to induce diuresis against water intoxication and cystic clot retention. This study was undertaken to compare the diuretic effects of glycerol with furosemide after TURP. METHODS: Thirty patients (ASA I or II) undergoing TURP were studied. Spinal anesthesia was induced with bupivacaine. At the end of prostatic resection, the patients were randomly allocated into two groups. In one group (n = 15) the patients received furosemide 30 mg i.v., while in the other group (n = 15) they received glycerol 0.5 g/kg i.v. Blood samples were collected for measurements of osmolality, hematocrit, sodium and glucose concentration before anesthesia and after surgery. Urine output was also recorded after surgery in each group. RESULTS: Plasma osmolality in glycerol group was higher than furosemide group at 30 min (295.3 +/- 10.6 vs. 283.8 +/- 5.6 mOsm/kg, p < 0.01) and 1 h after operation (294.9 +/- 8.7 vs 286.3 +/- 6.7 mOsm/kg, p < 0.01). Blood glucose was higher in glycerol group than that in furosemide group at 2 h after operation (195.6 +/- 121.9 vs 152.9 +/- 70.1 mg/dl, p < 0.05). Measured urine output was significantly greater in furosemide group at 30 min after operation (904.6 +/- 491.5 vs. 248.4 +/- 143.4 ml, p < 0.05) but was greater in glycerol group at 12 h after operation. CONCLUSIONS: Since urine output is significantly less in glycerol group at 1 h after operation, glycerol is inferior to furosemide for preventing cystic clot retention after TURP. But glycerol may protect against water intoxication better for its merit of producing higher plasma osmolality.

Aged↗
PubMed1997

Effects of the angiotensin converting enzyme (ACE) inhibitor, captopril, on the cardiovascular, endocrine, and renal responses to furosemide in conscious lambs.

To test the hypothesis that angiotensin II modulates the physiological responses to furosemide in the newborn, various parameters of cardiovascular, renal, and endocrine function were measured before and after iv injection of furosemide to eight conscious, chronically instrumented lambs in the presence and absence of the angiotensin converting enzyme (ACE) inhibitor, captopril. During ACE inhibition, the rise in heart rate and decrease in renal blood flow in response to furosemide did not occur, and the natriuretic and diuretic responses to furosemide were attenuated by approximately two-thirds. There was also an increase in the urinary excretion of prostaglandin F2 and prostaglandin F1 alpha as well as an increase in the excretion of prostaglandin E2 after furosemide, in the presence of ACE inhibition. Therefore, the cardiovascular, renal, and endocrine responses to furosemide in conscious lambs were significantly altered by ACE inhibition.

6-Ketoprostaglandin F1 alpha↗