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PubMed1993

Influence of alpha-receptor blockade on the time-dependent change in the effect of furosemide.

Influence of alpha-receptor blockade on the time-dependent change in the effect of furosemide (a loop diuretic agent) was examined. Furosemide (30 mg/kg) was given orally to the doxazosin (an alpha 1-blocker)- or vehicle-treated rats at 12 AM or 12 PM. Urine volume and urinary excretions of of sodium and furosemide for 8 hr were significantly greater at 12 AM than at 12 PM in the vehicle-treated animals. However, such time-dependent changes in these parameters disappeared in the doxazosin-treated rats. These results suggest that the alpha 1-receptor-mediated stimuli are involved in the mechanism of the time-dependent change in the effect of furosemide.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed1992

Intermittent administration of furosemide vs continuous infusion preceded by a loading dose for congestive heart failure.

Several reports have suggested that continuous intravenous administration of loop diuretics may be superior to intermittent administration. We performed a prospective randomized crossover study comparing intermittent intravenous administration (IA) of furosemide with continuous infusion following a single loading dose (LDCI) in nine patients with severe congestive heart failure. At the time of hospital admission, patients were randomly assigned to one of two treatment groups. One group (four patients) received an IV bolus injection of furosemide followed immediately by a continuous infusion for 48 h. The second group (five patients) was treated with three IV bolus injections a day for 48 h. Total doses of furosemide were equivalent in the two groups. After 48 h, each patient was crossed over to the other method and treated for an additional 48 h. LDCI produced significantly greater diuresis and natriuresis than IA (total urine output increased by 12 to 26 percent, total sodium excretion increased by 11 to 33 percent) (p less than 0.01). There were no significant differences in side effects between the two methods. These results indicate that LDCI may be a preferred method for administration of furosemide in patients with congestive heart failure.

Aged↗

PubMed1993

Inhaled furosemide prevents ultrasonically nebulized water bronchoconstriction in children with both atopic and nonatopic asthma.

To determine whether inhaled furosemide can modify the bronchoconstriction induced by ultrasonically nebulized distilled water (UNDW) in children with both atopic and nonatopic asthma, a single-blind, randomized, placebo-controlled study was undertaken. The UNDW inhalation challenge was performed in 21 asthmatic children (atopic, 14; nonatopic, 7; mean +/- SEM age, 11.5 +/- 0.5 years), who had a fall in FEV1 of at least 20 percent after distilled water inhalation. On separate days, these subjects underwent UNDW challenge test after inhalation of furosemide (10 mg/body square meters) or placebo (saline solution). Inhaled furosemide exerted a protective effect against bronchoconstriction induced by UNDW in children with both atopic and nonatopic asthma (p < 0.01, p < 0.05, respectively). These results indicate that the protective action of furosemide against UNDW-induced bronchoconstriction may be independent of its direct inhibitory effect on airway mast cell activation.

Administration, Inhalation↗

PubMed1987

Colloid osmotic pressure in pulmonary edema clearance with furosemide.

After tripling of baseline lung water (EVLW), decreasing wedge pressure (PWP) alone for two hours did not decrease EVLW. In 11 of 16 dogs, triple baseline EVLW and a decrease in plasma colloid osmotic pressure (COP) from 21.1 +/- 0.8 to 17.8 +/- 0.8 mm Hg resulted from left atrial balloon inflation at PWP of 28 to 30 mm Hg. With subsequent lowering of PWP to 10 mm Hg, intravenously administered furosemide (1 mg/kg) was given to these 11 dogs. One half hour after furosemide, shunt decreased slightly without decreasing EVLW in all 11 dogs, but by two hours, seven dogs (group 1) decreased EVLW (from 23.2 +/- 1.8 to 11.1 +/- 1.4 ml/kg) and shunt (37.4 +/- 2.0 to 12.9 +/- 2.9 percent), while four dogs (group 2) did not (EVLW: 22.3 +/- 1.4 to 22.5 +/- 0.6 ml/kg: shunt, 36.8 +/- 1.7 to 36.5 +/- 1.9 percent). Group 1 had diuresis, maintained normal blood urea nitrogen and creatinine levels, and increased COP from 17.7 +/- 0.7 to 23.6 +/- 0.5 mm Hg while group 2 was oliguric with elevated BUN and creatinine values and showed no change in COP (17.9 +/- 0.9 to 18.3 +/- 0.6 mm Hg) after furosemide. After decreasing PWP in massive pulmonary edema (triple baseline EVLW), furosemide appeared to enhance edema clearance by changes in COP with diuresis.

Animals↗

PubMed1986

The functional response to furosemide in a case of de Toni-Debre-Fanconi disease.

The case of a 13-year-old boy with the advanced clinical picture of the idiopathic DeToni-Debré-Fanconi syndrome is described, on whom acute studies of proximal tubular functions and of the effect of furosemide thereon were performed. Sodium bicarbonate loading corrected the hyperchloremic acidosis, but induced an increase of urinary bicarbonate loss of over 20% of the filtered amount. Furosemide corrected bicarbonate reabsorption in spite of the presence of metabolic alkalosis. The urinary excretion of alpha-amino nitrogen, glucose, and phosphates decreased and tubular reabsorption of the two latter increased under furosemide. On a chronic treatment with furosemide and dietary sodium chloride restriction, correction of hyperchloremic acidosis, hypophosphatemia and rickets was achieved.

Adolescent↗

PubMed1994

Aldosterone response to adrenocorticotrophin and furosemide in primary aldosteronism after prolonged spironolactone treatment.

We evaluated the effects of prolonged spironolactone treatment on aldosterone secretion in patients with primary aldosteronism. The patients were hospitalized and underwent a furosemide test with or without dexamethasone, as well as an adrenocorticotrophin (ACTH) test. In untreated patients, neither plasma renin activity (PRA) nor plasma aldosterone showed a response in the furosemide test. In patients receiving spironolactone, furosemide increased significantly both the PRA and the plasma aldosterone concentration (from 2.6 +/- 0.8 to 7.0 +/- 2.0 micrograms.l-1.h-1 (p < 0.05) and from 345.6 +/- 55.8 to 492.7 +/- 76.8 ng/l (p < 0.05), mean +/- SEM, respectively). Dexamethasone administration had no effect on the results of the furosemide test (p > 0.1). However, dexamethasone tended to decrease the basal plasma aldosterone concentration in the untreated patients, but not in the patients receiving spironolactone. In the ACTH test, the plasma aldosterone concentration increased significantly in the untreated patients (from 549.0 +/- 69.8 to 1169.3 +/- 165.5 ng/l, p < 0.01), but there was no significant aldosterone response in the spironolactone-treated patients (from 885.5 +/- 204.9 to 1260.3 +/- 289.2 ng/l, p > 0.1). We conclude that aldosterone secretion is mainly dependent on ACTH in the untreated patients with primary aldosteronism and is more strongly regulated by the renin-angiotensin system during spironolactone treatment.

Adrenocorticotropic Hormone↗

PubMed2000

Lack of renoprotective effects of dopamine and furosemide during cardiac surgery.

Because development of acute renal failure is one of the most potent predictors of outcome in cardiac surgery patients, the prevention of renal dysfunction is of utmost importance in perioperative care. In a double-blind randomized controlled trial, the effectiveness of dopamine or furosemide in prevention of renal impairment after cardiac surgery was evaluated. A total of 126 patients with preoperatively normal renal function undergoing elective cardiac surgery received a continuous infusion of either "renal-dose" dopamine (2 microg/kg per min) (group D), furosemide (0.5 microg/kg per min) (group F), or isotonic sodium chloride as placebo (group P), starting at the beginning of surgery and continuing for 48 h or until discharge from the intensive care unit, whichever came first. Renal function parameters and the maximal increase of serum creatinine above baseline value within 48 h (deltaCrea(max)) were determined. The increase in plasma creatinine was twice as high in group F as in groups D and P (P < 0.01). Acute renal injury (defined as deltaCreamax) >0.5 mg/dl) occurred more frequently in group F (six of 41 patients) than in group D (one of 42) and group P (zero of 40) (P < 0.01). (The difference between group D and group P was not significant.) Creatinine clearance was lower in group F (P < 0.05). Two patients in group F required renal replacement therapy. The mean volume of infused fluids, blood urea nitrogen, serum sodium, serum potassium, and osmolar- and free-water clearance was similar in all groups. It was shown that continuous infusion of dopamine for renal protection was ineffective and was not superior to placebo in preventing postoperative dysfunction after cardiac surgery. In contrast, continuous infusion of furosemide was associated with the highest rate of renal impairment. Thus, renaldose dopamine is ineffective and furosemide is even detrimental in the protection of renal dysfunction after cardiac surgery.

Acute Kidney Injury↗

PubMed1996

Auditory brainstem response (ABR) and effects of furosemide on ABR in conscious F344 rats.

The present study was conducted to evaluate the variations in the normal auditory brainstem response (ABR) between the F344 and Wistar rats. It was also investigated whether strain differences exist in the ABR profiles of each strain of rat given furosemide, which induced ototoxicity. The typical waveform of ABRs in the F344 rats were similar to those observed in the Wistar rats. There were no significant differences between the strains in almost all parameters, but peak latencies from P1 to P3 in the F344 rats tended to be longer than those in the Wistar rats. After a single intravenous injection of furosemide, the minimum effective dosage levels, at which each peak of the ABR disappeared, were 53.3 +/- 8.2 and 70.0 +/- 8.9 mg/kg in the F344 and Wistar rats, respectively. A single intravenous injection of 100 mg/kg furosemide delayed the reversal of decrease in amplitude, prolongation of peak latency and the reappearance time in F344 rats. Thus, the normal waveform of ABR was comparable in the F344 and Wistar rats, but a tendency towards a prolongation in each latency was noted in the F344 rat. The results also suggested that the ABR of F344 rats were more vulnerable to furosemide ototoxicity than that of Wistar rats.

Animals↗

PubMed2006

Furosemide, a blocker of Na+/K+/2Cl- cotransporter, diminishes proliferation of poorly differentiated human gastric cancer cells by affecting G0/G1 state.

Furosemide, a blocker of Na(+)/K(+)/2Cl(-) cotransporter (NKCC), is often used as a diuretic to improve edema, ascites, and pleural effusion of patients with cancers. The aim of the present study was to investigate whether an NKCC blocker affects cancer cell growth. If so, we would clarify the mechanism of this action. We found that poorly differentiated gastric adenocarcinoma cells (MKN45) expressed the mRNA of NKCC1 three times higher than moderately differentiated ones (MKN28) and that the NKCC in MKN45 showed higher activity than that in MKN28. A cell proliferation assay indicates that furosemide significantly inhibited cell growth in MKN45 cells, but not in MKN28 cells. Using flow cytometrical analysis, we found that the exposure to furosemide brought MKN45 cells to spend more time at the G(0)/G(1) phase, but not MKN28 cells. Based on these observations, we indicate that furosemide diminishes cell growth by delaying the G(1)-S phase progression in poorly differentiated gastric adenocarcinoma cells, which show high expression and activity of NKCC, but not in moderately differentiated gastric adenocarcinoma cells with low expression and NKCC activity.

Adenocarcinoma↗

PubMedDate not supplied

Cochlear damage resulting from kanamycin and furosemide.

Permanent cochlear damage has been shown to occur in guinea pigs following the combined administration of kanamycin and furosemide. At the doses used, only a transient effect was measured with furosemide alone and no effect was detectable with kanamycin alone. This interaction results when a single subcutaneous dose of 400 mg/kg of kanamycin is followed in 2 hours by a single intravenous dose of furosemide. The dosage range for furosemide was 50 mg/kg for a just-detectable effect to 100 mg/kg for a very severe effect. Damage to the cochlea was ascertained by measures of the a.c. cochlear potential as well as surface preparation histology.

Animals↗

PubMedDate not supplied

The furosemid test for Menière's disease.

In a previous report it was suggested that intravenous administration of furosemid followed by a comparative caloric test (the furosemid test) could be utilized for detection of endolymphatic hydrops (Kitahara et al., 1973). As a result of the further application of the furosemid test upon 161 patients with vertigo, positive results were observed in 80% of patients with typical Menière's disease, 6% of atypical Menière's disease, 42% with labyrinthine syphilis and 27% with sudden deafness. In patients with labyrinthitis, results were negative. It is thus concluded that the furosemid test provides positive evidence for determining the etiology of vertigo.

Audiometry↗

PubMed1977

Inhibition of furosemide-induced natriuresis by acetylsalicylic acid in dogs.

The effect of intravenously administered acetylsalicylic acid (ASA) has been investigated in two sets of experiments in conscious dogs. In the first part of the study ASA 70-90 mg/kg was infused for 40 min. Urine flow, free water clearance, renal blood flow and urinary excretion of sodium did not change significantly as compared to placebo treated animals. This is in contrast to the effects of comparable ASA doses in the pentobarbital anaesthetized dog. In the second part of the study the effects of pre-treatment with the same ASA doses of 5 ml 0.6% NaCl (placebo) on some renal effects of furosemide 1 mg/kg (intravenously) were investigated. In the placebo group acute furosemide treatment increased CIN in five out of six dogs and CPAH in all six dogs, these increases being most prominent the first 10 min after drug administration. After pre-treatment with ASA the initial increases in CIN and CPAH were almost abolished. CIN was reduced by 23.8% and CPAH by 30.6% during the first six clearance periods (0-6- min) after diuretic treatment in the ASA group as compared to the placebo group. Although urinary sodium excretion also increased in ASA pre-treated dogs, the effect of furosemide was greater in all dogs in the placebo group (P less than 0.05), and the effect of furosemide on fractional tubular reabsorption of sodium was significantly attenuated after pre-treatment with ASA.

Animals↗

PubMed1989

Precocious retinal adhesion is affected by furosemide and ouabain.

A "precocious" adhesive force develops between the neurosensory retina (NSR) and the retinal pigment epithelium (RPE) 15-30 minutes after eyes are removed from day 15 embryonic chickens and incubated at 37 degrees C. Precocious adhesion has been reported to be blocked by exposure to cold but to be unaffected by exposure to furosemide and ouabain. Since RPE transport is thought to play a major role in the adhesion between the RPE and NSR of adult mammals, and since ouabain and furosemide block RPE transport in embryonic chickens, it has been thought that precocious adhesion in embryonic chickens is not a good model for studying adhesion between the RPE and the NSR of adult mammals. We have found, however, that when steps are taken to ensure that ouabain and furosemide reach the transport sites on RPE apical membrane before precocious adhesion develops, that ouabain and furosemide do affect precocious adhesion.

Animals↗

PubMed1980

Furosemide, indomethacin and sodium excretion in isolated, blood-perfused dog kidneys.

Sodium excretion, renal blood flow and glomerular filtration rate were investigated in isolated, blood-perfused dog kidneys, thus excluding the interference of changes in body sodium and water balance. Four groups of experiments were performed : (a) control; (b) blood + indomethacin; (c) blood + furosemide; (d) blood + furosemide and indomethacin. The progressive vasodilatation due to the accumulation of prostaglandins was suppressed by indomethacin, the glomerular filtration rate remaining unchanged. The inhibition of prostaglandins synthesis was without influence on the natriuretic activity of furosemide. These results seem incompatible with an intrarenal mediation by prostaglandins of the diuretic effect of furosemide; moreover, this effect was dissociated from the changes in renal blood flow ascribed to renal prostaglandins.

Animals↗

PubMed1987

Effect on intracranial pressure of furosemide combined with varying doses and administration rates of mannitol.

The first part of this study investigated the combined use of furosemide and mannitol in the treatment of elevated intracranial pressure (ICP). Two groups of dogs were studied to determine if renal excretion of mannitol was altered in the presence of furosemide. No significant difference in excretion was noted between the two groups. Fifteen animals were used in other studies to identify the most advantageous sequence of administration of furosemide and mannitol. Infusion of mannitol followed by furosemide 15 minutes later resulted in the most profound and sustained ICP reduction. The effect on ICP reduction of varying the mannitol dose was observed in studies using single doses of 0.5 gm/kg, 0.75 gm/kg, and 1 gm/kg. The larger mannitol dose, resulting in a greater blood-brain osmotic gradient, proved to be the most efficacious in ICP reduction. A further 15 animals were used in investigations to determine whether changing the rate of delivery of the most effective mannitol dose (1 gm/kg) influenced resultant ICP reduction. The results indicated that rapid administration (2 ml/kg/min) produced higher peak serum concentrations of mannitol and more profound lowering of ICP than the same dose delivered at slower rates.

Animals↗

PubMed1975

Furosemide induced release of prostaglandin E to increase renal blood flow.

Levels of PGE in renal venous blood were found to be significantly elevated at the time RBF was increased by furosemide. Following indomethacin, a second dose of furosemide failed to increase RBF and levels of PGE in renal venous blood were not elevated. Levels of PGF and PGA were not affected by furosemide. The increase of PGE in renal venous blood at the time of renal dilation supports the hypothesis that furosemide increases RBF by releasing PGE. An intrarenal action of the released PGE is implied by this mechanism.

Animals↗

PubMed1984

Inhibition of furosemide-induced kaliuresis in the rat by trilostane, an inhibitor of adrenal steroidogenesis.

In rats treated with furosemide, urinary losses of water, sodium and potassium were accompanied by increased circulating levels of aldosterone. Trilostane, an inhibitor of adrenal 3 beta-hydroxysteroid dehydrogenase activity, prevented furosemide-induced hyperaldosteronism which resulted in a partial inhibition of diuretic-induced kaliuresis without a change in sodium and water excretion. Spironolactone, an antagonist of mineralocorticoid action with inherent diuretic activity, produced qualitatively similar effects to those of trilostane on urinary electrolyte excretion in furosemide-treated intact rats. However, mineralocorticoid-induced potassium loss in adrenalectomized rats was not altered by trilostane but was prevented by spironolactone reflecting the direct effect of spironolactone on the kidney. In addition, furosemide-induced kaliuresis in adrenalectomized rats was not prevented by trilostane. Therefore, although both trilostane and spironolactone reduce diuretic-induced potassium loss, spironolactone acts by competing with aldosterone for the mineralocorticoid receptor while trilostane appears to act exclusively by preventing secondary hyperaldosteronism.

3-Hydroxysteroid Dehydrogenases↗

PubMed2007

[Diuretic effect of injecting furosemide into low hydraulic resistance point Shuifen along the conception meridian in pigs with acute edema].

OBJECTIVE: To observe whether injection of medicine into low hydraulic resistance point along meridian brings about higher medicinal effect and to explore the efficacy of the theory that meridians are made up of channels featuring low hydraulic resistance by observing the diuretic effect of injecting furosemide or saline into the low hydraulic resistance point Shuifen (CV 9), vein and Zusanli (St 36) respectively. METHODS: Acute edema was induced in pigs by rapid intravenous injection of 2 000 ml normal saline. The pigs were divided into four groups: Shuifen (CV 9) injection of half dose furosemide group (SFF group), intravenous injection of full dose furosemide group (VF group), Zusanli (St 36) injection of full dose furosemide group (ZSLF group), and Shuifen (CV 9) injection of half dose normal saline group (SFS group). The accumulated urine quantity and the urine quantity generated in every 15-minute period were measured in each group respectively, every 15 minutes after injection, and the measurement lasted for two hours at one experiment. Each group involved eight times of experiments with one pig used for one experiment, which means the whole observation involved 32 times of experiments. RESULTS: The accumulated urine quantities observed in both SFF group and VF group were higher than those in the ZSLF group and the SFS group all through the measurement, showing significant differences during the period from the 15th minute to the 45th minute (P<0.05). But no significant difference was observed between the SFF group and the VF group during the whole 2-hour measurement (P>0.05). Analysis of urine quantity generated in every 15-minute period showed that diuretic effect climaxed during the 15th minute to the 30th minute in both SFF group and VF group. By contrast, ZSLF group reached diuresis climax during the 45th minute to 60th minute and no diuresis climax was observed in the SFS group all through the measurement. CONCLUSION: Injection of medicine into low hydraulic resistance point along meridian generates faster and more powerful medicinal potency, and this is likely to be applied to clinical practice. The theory that meridians are channels featuring low hydraulic resistance is important to the elucidation of meridians.

Acupuncture Points↗