Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FUROSEMIDE”

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

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

At least 1,027 records · Page 57Linked to original sources
PubMed2003

Furosemide loading vestibular evoked myogenic potential for unilateral Ménière's disease.

OBJECTIVE: To investigate whether endolymphatic hydrops in Ménière's Disease could be diagnosed by comparing vestibular evoked myogenic potential (VEMP) before and after furosemide administration (F-VEMP). STUDY DESIGN: Retrospective study. SETTING: University hospital. INTERVENTION: Furosemide administration. PATIENTS: Twenty-five affected ears of patients with unilateral Ménière's Disease were studied. The patients had received confirmed diagnoses Ménière's Disease; thus, the presence of endolymphatic hydrops was suggested. For the control, 22 ears of 11 normal healthy volunteers who had never had vertigo or hearing disturbance were used. MAIN OUTCOME MEASURE: The amplitude of the p13-n23 biphasic wave before and after furosemide administration. RESULTS: The amplitude of the p13-n23 biphasic wave was significantly enlarged in 7 of 18 cases in which it could be detected before diuretic loading. The biphasic waves appeared after diuretic loading in 3 of 7 cases in which it could not be recorded before loading. Thus, the positive ratio of F-VEMP for unilateral Ménière's Disease was considered to be 40% (10 of 25). The ratio was similar to that of the conventional examinations for endolymphatic hydrops such as the glycerol test, furosemide test, and electrocochleogram. CONCLUSION: The F-VEMP test may be useful in the diagnosis of endolymphatic hydrops.

Adult↗
PubMed2003

Three cases of cochleosaccular endolymphatic hydrops without vertigo revealed by furosemide-loading vestibular evoked myogenic potential test.

OBJECTIVE: To describe possible cases of cochleosaccular endolymphatic hydrops without vertigo. STUDY DESIGN: Retrospective case report. SETTING: University hospital. PATIENTS: Three patients with possible cochleosaccular hydrops without vertigo were studied. The basis of diagnosis was positive result of the furosemide-loading vestibular evoked myogenic potential test, no canal paresis in the caloric test, and recurrent cochlear symptoms or fluctuating low-tone hearing loss. CASE REPORT: In case 1, a 47-year-old woman had recurrent left aural fullness and tinnitus and a few weeks later complained of a floating sensation and could not stand up. The furosemide-loading vestibular evoked myogenic potential test showed a positive result in the left ear. In case 2, a 24-year-old woman complained of a backward falling sensation lasting several seconds; subsequently, a severe floating sensation persisted and she could not stand up for several days. Audiography showed fluctuating low-tone hearing loss in the left ear, and the furosemide-loading vestibular evoked myogenic potential test showed a positive result. In case 3, a 41-year-old woman had a floating sensation while walking and subsequently complained of tinnitus in the left ear. She could not stand up because of a severe floating sensation and, moreover, complained of a sudden falling sensation lasting for several seconds. The furosemide-loading vestibular evoked myogenic potential test indicated a positive result in the left ear. CONCLUSIONS: The patients in cases 2 and 3 complained of a short-lasting sensation of falling down. Severe disequilibrium that prohibited standing up was noted in all cases. It was suggested that these symptoms were caused by saccular hydrops.

Adult↗
PubMed2005

Postpartum preeclampsia management with furosemide: a randomized clinical trial.

OBJECTIVE: This investigation was undertaken to estimate whether a brief postpartum course of furosemide for patients with preeclampsia benefits recovery and shortens hospitalization by enhancing diuresis, lessening severe hypertension, and reducing the need for antihypertensive therapy. METHODS: Two hundred sixty-four patients with preeclampsia were enrolled. After spontaneous onset of postpartum diuresis and discontinuation of intravenous magnesium sulfate, patients were randomly assigned to receive either no therapy or 20 mg oral furosemide daily for 5 days with oral potassium supplementation. Patient outcomes were compared between treatment groups with regard to classification of hypertensive disease. RESULTS: Only postpartum patients with severe preeclampsia (n = 70) who received furosemide compared with controls had significantly lower systolic blood pressure by postpartum day 2 (142 +/- 13 mm Hg compared with 153 +/- 19 mm Hg, P < .004) and required less antihypertensive therapy during hospitalization (14% compared with 26%, P = .371) and at discharge (6% compared with 26%, P = .045). No benefit was shown for patients with mild preeclampsia (n = 169) or superimposed preeclampsia (n = 25). Neither length of hospitalization nor frequency of delayed postpartum complications was positively affected by the intervention. CONCLUSION: Brief postpartum furosemide therapy for patients with severe preeclampsia seems to enhance recovery by normalizing blood pressure more rapidly and reducing the need for antihypertensive therapy. Shortening of hospitalization and reduction of delayed postpartum complications were not benefitted.

Adult↗
PubMed2005

A randomized, controlled trial of furosemide with or without albumin in hypoproteinemic patients with acute lung injury.

OBJECTIVE: Hypoproteinemia is a common condition in critically ill patients, associated with the development of acute lung injury and acute respiratory distress syndrome and subsequent worse clinical outcomes. Albumin with furosemide benefits lung physiology in hypoproteinemic patients with acute lung injury/acute respiratory distress syndrome, but the independent pharmacologic effects of these drugs are unknown. DESIGN: Randomized, double-blinded, placebo-controlled multicentered trial. SETTING: Eleven medical, surgical, and trauma intensive care units including 190 beds within two university hospital systems. PATIENTS: Forty mechanically ventilated patients with acute lung injury/acute respiratory distress syndrome, whose serum total protein concentrations were <6.0 g/dL were included. Patients were excluded for hemodynamic instability or significant renal or hepatic failure. INTERVENTIONS: Subjects were equally randomly allocated to receive furosemide with albumin or furosemide with placebo for 72 hrs, titrated to fluid loss and normalization of serum total protein concentration. MEASUREMENTS AND MAIN RESULTS: The primary outcome was change in oxygenation from baseline to day 1, with secondary physiologic and clinical outcomes. There were no differences in baseline characteristics of the subjects in relation to group assignment. Albumin-treated patients had greater increases in oxygenation (mean change in Pao2/Fio2: +43 vs. -24 mm Hg at 24 hrs and +49 vs. -13 mm Hg at day 3), serum total protein (1.5 vs. 0.5 g/dL at day 3), and net fluid loss (-5480 vs. -1490 mL at day 3) throughout the study period (all p < .05). Fluid bolus administration to control patients reduced net negative fluid balance; control patients more frequently developed hypotension and had fewer shock-free days, which translated to differences in organ failure at study end. CONCLUSIONS: The addition of albumin to furosemide therapy in hypoproteinemic patients with acute lung injury/acute respiratory distress syndrome significantly improves oxygenation, with greater net negative fluid balance and better maintenance of hemodynamic stability. Additional randomized clinical trials are necessary to examine mechanisms and determine the effect on important clinical outcomes, such as the duration of mechanical ventilation.

Combined Modality Therapy↗
PubMed2006

Antihypertensive drugs clonidine, diazoxide, hydralazine and furosemide regulate the production of cytokines by placentas and peripheral blood mononuclear cells in normal pregnancy.

BACKGROUND: Antihypertensive drugs such as clonidine, diazoxide, hydralazine and furosemide are used in the hypertensive disorders of pregnancy to control blood pressure, but it is not clear if they modulate the production of placental or circulating cytokines. OBJECTIVE: To examine the effect of pharmaceutical doses of well known antihypertensive drugs used for blood pressure control on the production of the cytokines interleukin (IL)-6, IL-10 and tumour necrosis factor (TNF)-alpha in placental tissue and peripheral blood mononuclear cells (PBMCs) in normal pregnancy. DESIGN: Placental biopsies were taken from the decidual surface of placentas after delivery of normal pregnancies (n = 6) and PBMCs were separated from the whole blood of normal term pregnant women (n = 7). Both villous explants and PBMCs were cultured with increasing concentrations of antihypertensive drugs. The dose effect of drugs on the production of placental and circulating cytokines (IL-6, IL-10 and TNF-alpha) were examined by enzyme-linked immunosorbent assay. RESULTS: Placental production of IL-10 was not affected by clonidine, but decreased significantly after incubation of the tissue with diazoxide, hydralazine or furosemide. Production of IL-10 by PBMCs increased significantly: by from 3.4 +/- 2.7% [16.3 pg/ml (range 6.1-21.5 pg/ml)] to 24.5 +/- 3.3% [30.4 pg/ml (range 16.9-34.8 pg/ml)] with increasing concentrations of clonidine (0.08-1.3 microg/ml), and by 8.8 +/- 3.5% [4.1 pg/ml (range 3.0-17.8 pg/ml)] and 17.2 +/- 1.9% [22.6 pg/ml (range 13.2-23.2 pg/ml)] with lower doses of hydralazine (6.3 and 12.5 microg/ml) (all P values < 0.05). There was a stepwise reduction in production of TNF-alpha and IL-6 with increasing doses of diazoxide, hydralazine and furosemide by placentas and PBMCs from these women with normal pregnancies. CONCLUSION: Our data suggest that the antihypertensive drugs clonidine and hydralazine can stimulate production of the circulating anti-inflammatory cytokine IL-10, whereas furosemide and diazoxide inhibit the production of this cytokine and the proinflammatory cytokines TNF-alpha and IL-6 by placentas and PBMCs.

Antihypertensive Agents↗
PubMed1981

Effects of furosemide and orthostasis on active and inactive renin in normal and anephric man.

We investigated active and inactive (acid-activatable) plasma renin in anephric and in normal persons. In anephric patients (n = 15) plasma concentration of active and inactive renin was 1.15 +/-- 0.2 and 40.7 +/- 7.1 microunits ml, respectively; angiotensin II (n = 13) was 14.5 +/- 1.9 pg/ml. Furosemide (n = 10), 40 mg i.v., and upright posture (n = 8) did not change active or inactive renin in the anephric state. In normal men, furosemide (n = 9) within 15 min increased active renin from 29.9 +/- 5.8 to 82.4 +/- 14.8 microunits/ml (P less than 0.001), while inactive renin slightly but not significantly decreased from 136.3 +/- 29.9 to 121.1 +/- 19.2 microunits/ml; orthostasis (n = 15) within 4 h stimulated active renin (P less than 0.001) and slightly raised inactive renin (P less than 0.05). Both furosemide and orthostasis increased (P less than 0.001 each) the proportion of active renin in normal persons. Studies in one patient within 24 h after bilateral nephrectomy indicated half-life to be 30-60 min for active and 2-4 h for inactive renin. Thus, we detected low levels of active renin and considerable amounts of inactive renin and angiotensin II in anephric patients. Our data suggest that about 30% of inactive renin in normal plasma is of extrarenal origin. The stimulation of active renin by furosemide and orthostasis is bound to the presence of the kidney. Our studies provide indirect evidence that both manoeuvres may stimulate the conversion of inactive to active renin within the human kidney.

Adult↗
PubMed1995

Effects of water deprivation for 48 hours on the pharmacokinetics and pharmacodynamics of furosemide in rats.

The effects of water deprivation for 48 h on the pharmacokinetics and pharmacodynamics of furosemide were examined after intravenous, 8 mg/kg body weight, and oral administration, 16 mg/kg body weight, of furosemide to control and water deprived rats. After i.v. administration, the total body and nonrenal clearances decreased significantly in water-deprived rats. The urine output, urinary excretion of sodium, potassium and chloride based on grams of kidney weight, and the diuretic, natriuretic and chloruretic efficiencies decreased significantly in water-deprived rats after both intravenous and oral administration of furosemide, suggesting that the dose of furosemide for water-deprived patients may require modification.

Administration, Oral↗
PubMed1996

Prolonged-release hydroxypropyl methylcellulose matrix tablets of furosemide for administration to dogs.

Furosemide is a problematic drug in a prolonged-release product because its absorption is site specific, taking place mainly in the upper parts of the alimentary tract. The aim of the study reported here was to develop prolonged-release furosemide formulations for dogs. The type of preparation selected was a hydroxypropyl methylcellulose (HPMC) matrix tablet. Evaluation was based on dissolution studies, on in vivo disintegration studies in the canine stomach and on bioavailability studies in Beagle dogs. The variables tested were the viscosity grade of the polymer, the amount of polymer and presence or absence of an alkaline compound (potassium carbonate) in the formulation. When potassium carbonate was included, furosemide was absorbed so slowly that drug administration once daily would give plateau drug plasma concentrations, even though the elimination half-life of furosemide is only about one hour. In vitro dissolution tests gave a wrong indication of the in vivo behaviour of the products. Thus, in vivo studies are important from the very beginning in the development of new drug products for dogs.

Absorption↗
PubMed1993

Potentiation of the antireactive, antiasthmatic effect of inhaled furosemide by inhaled lysine acetylsalicylate.

Nonsteroid antiinflammatory drugs interfere with the diuretic activity of furosemide, implying that this effect is at least partially dependent on renal prostaglandin synthesis. To investigate whether prostaglandin production could also modulate the bronchial antireactive activity of this diuretic drug, we investigated the effect of inhaled lysine acetylsalicylate (162 mg) and of furosemide (18 mg), alone and in combination, on the bronchial obstructive response to ultrasonically nebulized water in asthmatic patients. The study was also prompted by the conflicting results obtained in previous studies of oral nonsteroid antiinflammatory drugs. Fifteen asthmatic patients underwent bronchial challenge with a mist of ultrasonically nebulized distilled water at the same time of day on four occasions, 2-4 days apart, 15 min after premedication according to a double-blind, randomized protocol. After placebo, mean PD15 to water mist did not differ from a preliminary test (2.1 +/- 0.2 and 2.5 +/- 0.4 ml, M +/- SE, respectively). After lysine acetylsalicylate, mean PD15 rose to 5.0 +/- 0.7 ml (2.8 +/- 0.6 times higher than placebo); after furosemide, to 9.0 +/- 1.5 ml (4.4 +/- 0.9 times over placebo); and after the two drugs in combination, to 32.2 +/- 5.6 ml (16.3 +/- 3.0 times higher than placebo). Similar results were obtained with inhaled indomethacin, whereas sodium salicylate had no effect. These data indicate that the bronchial antireactive activity of inhaled furosemide is greatly enhanced by inhaled lysine acetylsalicylate through a mechanism which probably involves inhibition of the local synthesis of prostaglandins, and could have therapeutic implications.

Administration, Inhalation↗
PubMed1991

Furosemide inhibits the centrally-mediated pressor response to clonidine in conscious, normotensive rats.

1. The effect of furosemide on the pressor response induced by intracerebroventricular (i.c.v.) injection of clonidine was investigated in freely moving, normotensive rats with chronically implanted arterial catheters. 2. When injected i.c.v., clonidine at doses of 5 and 10 micrograms produced a dose-dependent pressor response and a decrease in heart rate. No depressor response was induced by clonidine. 3. Systemic (i.v.) pretreatment with furosemide (2-10 mg kg-1) increased urine volume and dose-dependently inhibited the pressor response to i.c.v. clonidine (10 micrograms), and a long-lasting depressor response to clonidine was observed. However, furosemide treatment did not alter the bradycardia produced in response to clonidine. 4. The systemic treatment with furosemide (10 mg kg-1, i.v.) had no effect on the pressor response to i.v. noradrenaline. 5. These results suggest that reduction of body fluid volume inhibits the centrally-mediated pressor response to clonidine and leads to the hypotensive effect. We also suggest that combined treatment with a diuretic increases the hypotensive efficacy of clonidine.

Animals↗
PubMed2005

Treatment of hepatorenal syndrome as defined by the international ascites club by albumin and furosemide infusion according to the central venous pressure: a prospective pilot study.

OBJECTIVE: Hepatorenal syndrome (HRS) is a functional renal failure that occurs late during cirrhosis. The prognosis is extremely poor with a mean survival of 1.7 wks from the time of diagnosis. The aim of the present study was to examine the effects of albumin and furosemide administration tailored to central venous pressure (CVP) on renal function and clinical outcome. METHODS: We treated 20 consecutive patients with HRS. Albumin was given to increase and/or maintain CVP above 3 cm H(2)O. If diuresis remained below 50 mL/h despite effective volume expansion, furosemide was administrated. Patients were considered responders and treatment was discontinued when creatinine clearance rose above 40 mL/min or serum creatinine fell under 132 mumol/L. RESULTS: The need for albumin varied from patient to patient (extremes 40-600 g) and in the same patient from day to day. All but one needed furosemide. Eleven patients (55%) responded to treatment. In this population, diuresis, serum creatinine, and creatinine clearance were all significantly improved. Creatinine clearance at baseline was predictive of treatment efficacy. Survival increased in these patients compared to nonresponders defined as patients with no improvement in renal function (259 days +/- 113 compared to 14 days +/- 3, p < 0.0005). Response to treatment and the type of HRS were the only variables with an independent prognostic value. CONCLUSION: This study shows that HRS as defined by the International Ascites Club can be treated by albumin administration alone or with furosemide given according to the patient's specific need using CVP.

Adult↗
PubMed1989

Effects of furosemide on the oral cavity.

Furosemide, a potent loop diuretic, has been reported to cause xerostomia, a sensation of oral dryness. We obtained urine and salivary secretions from five normal males after oral intake of either 0.5 mg/kg body weight of furosemide or placebo. The experimental treatment resulted in a five-fold increase in urinary output. In contrast, analysis of salivary secretions indicated there were no significant differences in flow rates, total output, total protein, or Na+, K+, or Cl- concentrations following drug or placebo. Subjectively, xerostomia was experienced 10 times more frequently after ingestion of furosemide. These data suggest that, in vivo, furosemide had a greater effect on the kidney than on the salivary gland and that the sensation of oral dryness is not solely a function of the quantitative salivary output.

Adult↗
PubMed1979

Different effects of furosemide on urinary excretion of prostaglandin E2 and F2 alpha in rabbits.

The effect of a constant infusion of furosemide (130 micrograms/min i.v. for 60 min, n = 8) was studied on urinary excretion of water, electrolytes and immunoreactive prostaglandin E2 (iPGE2) and iPGF2alpha in chloralose-urethane anesthetized rabbits. During the furosemide infusion sodium and water excretion increased ten-fold and the excretion of potassium and iPGE2 two to three times. The excretion of iPGF2alpha (0.06 +/- 0.03 micrograms/min/100 g kidney weight) was not significantly changed during the furosemide infusion but increased markedly after the infusion and reached a maximum (1.0 +/- 0.6 microgram/min/100 g) 30 to 45 min later, while the small increase in iPGE2 excretion at this time could be attributed to cross-reaction with PGF2alpha. The results indicate that PGE2 might possibly be involved directly in the action of furosemide, while PGF2alpha might participate in sodium and water conserving mechanisms in the rabbit kidney, activated by the drug induced diuresis.

Animals↗
PubMed1998

Evaluation of oral mucoadhesive microspheres in man on the basis of the pharmacokinetics of furosemide and riboflavin, compounds with limited gastrointestinal absorption sites.

When sustained-release adhesive and non-adhesive microspheres which release the same drugs at similar rates are administered orally, drug absorption after administration of adhesive microspheres should, if the gastrointestinal residence of adhesive microspheres is prolonged as a result of mucoadhesion, be higher than that after administration of non-adhesive microspheres. The gastrointestinal transit of oral adhesive microspheres in man has been evaluated pharmacokinetically using furosemide and riboflavin, compounds with limited absorption sites in the upper small intestine. In a preliminary experiment with fasted rats it was confirmed that a higher percentage of the drug remained in the stomach and that plasma drug levels were higher when furosemide was administered in the form of adhesive rather than non-adhesive microspheres. Two kinds of sustained-release microsphere, adhesive and non-adhesive, containing furosemide and riboflavin in hard gelatin capsules were prepared and orally administered to 10 healthy fasted volunteers in a cross-over design. Areas under the plasma concentration-time curves (AUC) were 1.8 times larger for furosemide and urinary recovery was 2.4 times higher for riboflavin when adhesive microspheres rather than when non-adhesive microspheres were used. When adhesive microspheres containing riboflavin were administered to fed volunteers, urinary recovery was 2.1 times higher and mean residence time (MRT) was more prolonged than when the microspheres were administered to fasted volunteers. Adhesive microspheres were found to adhere to the gastric or intestinal mucosa with high affinity in man and rats, resulting in prolonged gastrointestinal residence.

Adhesives↗
PubMed1983

Furosemide fails to alter plasma active or inactive renin in conscious sheep but does so in anaesthetized animals.

Regulation of plasma levels of active and inactive renin was investigated using sheep with indwelling artery, vein and bladder catheters. Control and experimental studies were carried out in the same animals on different days. Volume depletion during any single experiment was limited to a maximum of 50 ml. Despite large changes in sodium and water excretion, the diuretic furosemide at two dose levels, 1 and 10 mg/kg, failed to alter plasma levels of either active or inactive renin in conscious sheep. Induction of pentobarbitone anaesthesia in the sheep did not, per se, alter either plasma active or inactive renin. Furosemide (10 mg/kg) in anaesthetized animals produced a similar diuresis and natriuresis response to conscious sheep, but plasma active renin increased by 270% and inactive renin decreased to zero. In conscious sheep given an infusion of papaverine, furosemide also produced an increase in plasma active renin and a concurrent decrease in the inactive form. In both anaesthetized animals and in conscious sheep infused with papaverine, furosemide-induced intrarenal vasodilation, as evidenced by changes in clearance of p-aminohippuric acid, was much reduced in comparison to the conscious animals. This may be significant in relation to the control of renin secretion. It appears that the macula densa sodium receptor, which is considered to regulate renin release, will only function after it has been primed by other intra- or extrarenal factors. This is discussed, particularly in relation to the possible role played by the prostaglandin system.

Anesthesia, Intravenous↗
PubMed1984

The effect of furosemide on sodium movements in human red blood cells.

A study has been made of Na movements in human red blood cells in order to test their sensitivity to inhibition by furosemide or bumetanide. Net changes as well as influx and efflux were measured. Unidirectional Na influx and efflux values confirmed previous evidence for components of both these fluxes sensitive to inhibition by furosemide or bumetanide. The difference between furosemide-sensitive unidirectional influx and efflux was determined at [Na]o 140 mM and shown to be non-significant, even when [Na]i was raised to about 45 mumol ml cells-1. No evidence was found for an influence of furosemide on net movements of Na in cells of either slightly elevated or physiological [Na]i incubated in a 140 mM-Na medium over 4 h. Incubation of cells, under similar conditions, for 12 h did not reveal a bumetanide-sensitive net Na movement. The results suggest that cells with normal or slightly elevated [Na]i, incubated in media of physiological Na concentration, do not possess a mechanism sensitive to inhibition by the loop diuretics that operates to regulate cell Na.

Biological Transport, Active↗
PubMed1995

Dissociation of synchronization and excitability in furosemide blockade of epileptiform activity.

Furosemide, a chloride cotransport inhibitor, reversibly blocked synchronized burst discharges in hippocampal slices without reducing the pyramidal cell response to single electrical stimuli. Images of the intrinsic optical signal acquired during these slice experiments indicated that furosemide coincidentally blocked changes in extracellular space. In urethane-anesthetized rats, systemically injected furosemide blocked kainic acid-induced electrical discharges recorded from cortex. These results suggest that (i) neuronal synchronization involved in epileptiform activity can be dissociated from synaptic excitability; (ii) nonsynaptic mechanisms, possibly associated with furosemide-sensitive cell volume regulation, may be critical for synchronization of neuronal activity; and (iii) agents that affect extracellular volume may have clinical utility as antiepileptic drugs.

4-Aminopyridine↗
PubMed1976

Vascular actions of furosemide and bumetanide on the rat superior mesenteric vascular bed: interactions with prolactin and prostaglandins.

The mesenteric vascular bed of the rat was used to investigate the effects of furosemide, bumetanide, prolactin, aspirin, indomethacin and prostaglandin E2 on the pressor response to norepinephrine. Furosemide, bumetanied and indomethacin could all inhibit the responses to norepinephrine: in each case responsiveness was restored by the addition of prostaglandin E2 to the perfusate. Bumetanide and furosemide both failed to inhibit responsiveness in the presence of an adequate amount (50 pg/ml) of prostaglandin E2. As has been shown previously, ovine prolactin in a concentration of 50 ng/ml enhanced pressor responses to norepinephrine while 500 ng/ml, after an initial potentiation, inhibited responsiveness. Aspirin, furosemide and bumetanide all reversed both the potentiation produced by the lower prolactin concentration and the inhibition produced by the higher one. When taken in conjunction with other evidence these results suggest that the diuretics exert their vascular effects by inhibiting prostaglandin synthesis whereas prolactin acts by stimulating such synthesis.

Animals↗