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PubMed1983

Treatment of severe hypertension with labetalol compared with methyldopa and furosemide. Results of a long-term, double-blind, multicenter trial.

Eighty-one severely hypertensive patients were enrolled in a multicenter, double-blind, parallel group study evaluating the efficacy and safety of labetalol alone or in combination with furosemide versus methyldopa in combination with furosemide. A one day to four week placebo lead-in phase was followed by a one- to six-week titration period and a one-year maintenance period. Treatment with labetalol alone or in combination with furosemide, as well as methyldopa plus furosemide, was associated with significant reductions in supine and standing blood pressure levels. Moreover, after six months and one year of treatment, respectively, labetalol caused a significantly (p less than 0.05) greater reduction in the systolic blood pressure than the methyldopa regimen. The antihypertensive effect of labetalol was associated with small, yet significant reductions in heart rate; in contrast, resting tachycardia was observed in methyldopa-treated patients. Side effect profiles of the two treatments were different, with nausea being the most commonly reported side effect during labetalol therapy, and asthenia, somnolence, and dry mouth during methyldopa therapy. Overall, 33 of 65 (53 percent) labetalol-treated and 28 of 60 (47 percent) methyldopa-treated patients had at least a good response (that is, standing diastolic blood pressure 90 to 94 mm Hg) to therapy, including 26 (40 percent) and 22 (37 percent) patients, respectively, who had standing diastolic blood pressure levels of less than 90 mm Hg. Thus, labetalol is a potentially safe and effective agent in the long-term management of the patient with severe hypertension.

Adult↗
PubMed1984

Blood volume following diuresis induced by furosemide.

Changes in blood volume were investigated following intravenous injection of a single dose of furosemide in 21 patients with pulmonary edema. In a subset of 10 patients in whom the blood urea nitrogen level was 11.4 +/- 2.2 mg/dl and the serum creatinine level was 1.3 +/- 0.1 mg/dl and in whom total urine output exceeded 1 liter over a four- to six-hour interval ("diuretic" group), no significant change in plasma or total blood volume was observed, nor were there any significant changes in hematocrit. In a "nondiuretic" group of 11 patients who had moderately decreased renal function (blood urea nitrogen level 59.3 +/- 13.0 mg/dl and serum creatinine level 2.3 +/- 0.3 mg/dl) and in whom total urine output was less than 1 liter over the four- to six-hour interval, there was a significant increase in blood volume with a concomitant decrease in hematocrit and hemoglobin levels. Furosemide-induced diuresis therefore did not deplete intravascular volume. To the contrary, actions of furosemide that were independent of its diuretic action were associated with an expansion of plasma volume in the absence of diuresis. This may be related to the venous capacitance effects of furosemide with lowering of venous resistance and, therefore, lowering of the capillary hydrostatic pressure. In addition, there was an increase in colloid osmotic pressure. Both mechanisms increase the effective oncotic pressure gradient, which favors reabsorption of extravascular (edema) fluid. It is concluded that intravascular volume was therefore replenished at a rate equal to or in excess of the volume removed by diuresis.

Adult↗
PubMed1981

The effect of furosemide and bumetanide on cerebrospinal fluid formation.

Complete inhibition of carbonic anhydrase maximally reduces CSF flow 40-60%. We have confirmed that CSF flow in rabbits may be maximally decreased in this way by acetazolamide 30 mg/kg i.v., but have found only about 20% reduction from control after furosemide at 50 mg/kg i.v. This effect of furosemide is consistent with specific but partial inhibition of carbonic anhydrase of choroid plexus (and perhaps other sites of CSF secretion) based on the affinity of furosemide for carbonic anhydrase. Bumetanide, with 7 times lower affinity for carbonic anhydrase and 14-40 times higher inhibition of renal electrolyte transport processes than furosemide, did not decrease CSF flow.

Acetazolamide↗
PubMed1976

Reduction by indomethacin of furosemide effects in the rabbit.

The effects of furosemide on urine flow, sodium and potassium excretion and on plasma renin activity (PRA) were studied in anesthetized rabbits with and without pretreatment with indomethacin 5 mg/kg. Furosemide caused a 10-fold increase in urine flow and in sodium excretion, and a 2-3 fold increase in PRA. Pretreatment with the prostaglandin synthesis inhibitor, indomethacin, reduced the effects of furosemide on diuresis and on electrolyte excretion by over 80% (p less than 0.01) and PRA did not increase over the initial level. The results suggest that the effects of furosemide on PRA and on urinary sodium excretion may be related to the intrarenal activation of the prostaglandin system.

Animals↗
PubMed1995

Furosemide inhibits bradykinin-induced contraction of human bronchi: role of thromboxane A2 receptor antagonism.

Bradykinin contracts human isolated small bronchi through prostanoid release and subsequent TP receptor stimulation. Furosemide 10(-4) to 10(-3) M concentration dependently inhibited bradykinin- and the stable TP receptor agonist U-46619-induced contraction of human isolated small airways. The inhibitory effect of furosemide on U-46619-induced contraction involves competitive antagonism at TP receptors. Such an inhibition of TP receptors could a least partly explain the inhibitory effect of furosemide on bradykinin-induced contraction, and could be one of the mechanisms of the protective effect of furosemide in asthma.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1987

Immediate effects of furosemide on renal hemodynamics in chronic liver disease with ascites.

Furosemide occasionally causes azotemia in patients with ascites, independently of induced volume depletion. To define this effect, we measured renal clearances in patients with chronic liver disease and ascites and in nonascitic controls. Furosemide (80 mg i.v.) transiently increased p-aminohippurate clearance in controls (from 693 +/- 67 to 928 +/- 93 ml/min) and in 11 patients with ascites (from 418 +/- 81 to 526 +/- 80 ml/min). In contrast, in 13 patients with ascites, p-aminohippurate clearance fell by 34% (from 545 +/- 51 to 360 +/- 24 ml/min) within 20 min and by 41% within 60 min, and inulin clearance fell by 19% at 20 min and by 30% at 60 min. The renal effects lasted approximately 4 h. The renal response could not be predicted by renin activity, urinary prostaglandin excretion, urinary sodium, or clinical characteristics. In all 14 patients who received oral furosemide, p-aminohippurate clearance fell within 90 min (by 24%) and remained suppressed for at least 4 h. These immediate effects of furosemide on renal perfusion may contribute to azotemia in some patients with ascites.

Ascites↗
PubMed1991

Experimental evaluation of furosemide renography in unobstructed and partially obstructed upper urinary tracts in pigs.

To evaluate the reliability and the constancy of the furosemide renography an experimental evaluation of the test has been performed. A standardized unilateral partial proximal ureteral obstruction was applied to 11 pigs. Preoperatively and again weekly in the three weeks following obstruction a furosemide renogram (FR) was done. The furosemide renography was a very constant parameter in the unobstructed kidney (85%) and in the partly obstructed kidney (85%). A type I FR pattern (O'Reilly classification) was an exact indicator of an unobstructed pelvis. After partial ureteral obstruction, an immediate change in the FR pattern was seen either into type II or type IIIa renography. In this experimental study furosemide renography was found to be a reliable tool in the differentiation between the unobstructed normal renal pelves and the partly obstructed dilated renal pelves.

Animals↗
PubMed1978

Furosemide exhibits physicochemical properties similar to prostaglandins and interferes with their bioassay.

The parallel pharmacological assay system has been of inestimable value in the identification and quantification of prostaglandins. A greater degree of specificity is conferred on the bioassay system by the preparative techniques of extraction and chromatography, for substances which might interfere with the assay of prostaglandins are usually eliminated by these procedures. It would be highly unlikely for a substance to survive the extraction procedure, to exhibit chromatographic properties similar to the prostaglandins and to interfere with their bioassay. We report here such an occurrence. Thus, furosemide not only survived the acidic lipid extraction, but, in addition, it exhibited chromatographic properties identical to those of the prostaglandins of the E series and finally, furosemide, at a dose which in and of itself was without effect on the assay tissues, inhibited the responses to prostaglandins. The quantification of prostaglandins by radioimmunoassay was, on the other hand, not altered by the presence of furosemide. This latter method appears to be the one of choice when interrelations between prostaglandins and furosemide are being examined.

Animals↗
PubMed1978

The lack of an effect of furosemide on uterine prostaglandin metabolism in vivo.

We determined the effect of 2 mg/kg intravenous furosemide on the production and metabolism of prostaglandin E2 in the utero-placental unit of pregnant dogs. Uterine venous prostaglandins E2 and 15-keto-13,14-dihydro E2 were measured by gas chromatography-mass spectrometry. Even though the dose of furosemide was adequate to effect a good diuresis, neither the production nor the metabolism of prostaglandin E2 by the uterus was altered by that dose of the drug. Using radioactive microspheres to measure hemodynamic parameters, we observed no change in uterine vascular resistance while renal vascular resistance decreased. Although the renal concentration of furosemide may be higher than the uteroplacental concentration, there is so far no evidence in vivo that usual doses of furosemide enhance the production or inhibit the metabolism of prostaglandin E2.

Animals↗
PubMed1994

Characterization of monoclonal anti-furosemide antibodies and molecular modeling studies of cross-reactive compounds.

Four mouse monoclonal antibodies directed against furosemide have been isolated and characterized. The cross-reactivity of the antibodies with eight compounds which are structurally and/or functionally related to furosemide was determined using a competition ELISA. All of the compounds, including furosemide, were then modeled using molecular mechanical and quantum mechanical methods in an attempt to correlate antibody binding with the conformational and electronic properties of the molecules. The results of these experiments demonstrated that all of the cross-reactivity observed could be readily explained using these techniques. Furthermore, these results should allow for more accurate prediction of unexpected cross-reactivities with these antibodies when they are used in immunoassays for determination of furosemide.

Animals↗
PubMed1991

Role of dopamine1-receptors in mediating renal responses to furosemide in the rat.

1. Dopamine (DA) infusion enhanced the diuresis, natriuresis and kaliuresis evoked by furosemide, but this increase was significantly lower in the presence of SCH 23390, a selective DA1-dopaminergic antagonist. 2. Water, Na+ and K+ excretion induced by furosemide were reduced by haloperidol, and SCH 23390, whereas they were not affected by +/- sulpiride, a preferentially DA2-dopaminergic antagonist. 3. The treatments used did not modify the mean blood pressure during the experiments. 4. Our data show that renal responses to furosemide are attenuated by the DA1-dopaminergic antagonist. It is possible that endogenous DA, stimulating DA1 receptors in the rat kidney may be an important factor involved in the Na+, K+ and water excretion evoked by furosemide.

Animals↗
PubMed1994

Variation of distortion product otoacoustic emissions with furosemide injection.

Cochlear function was monitored in adult gerbils using distortion product otoacoustic emissions (DPOAE) during intraperitoneal injection of furosemide. All stimulus parameters were varied independently over a wide range, the stimulus frequencies f1 and f2 from 1 to 16 kHz, and the stimulus levels L1 and L2 from 20 to 80 dB SPL. The observed emissions at 2f1-f2 and 3f1-2f2 could be considered to be made up of two distinct components: (1) an 'active' source which depended in a complex way on the stimulus frequencies and levels, which was dominant at low and moderate stimulus levels, and which, by definition, was eliminated by sufficient furosemide intoxication; and (2) a 'passive' source which was essentially the same at all frequencies, with a level dependence given approximately by a simple power law distribution. The change from the active to the passive source was usually accompanied by an abrupt shift in emission phase angle. A simple summation model was shown to account for the observed form of this transition. The amount of the decrease in 2f1-f2 emission amplitude after furosemide injection was approximately independent of frequency and consistent for the middle frequency ratios and intensity levels (f2/f1 approximately equal to 1.3, L1 x L2 approximately equal to 55 x 50 dB SPL). It was concluded that the combination of DPOAE with furosemide injection can usefully be employed as a probe of active cochlear mechanics.

Acoustic Stimulation↗
PubMed1992

Furosemide decreases eggshell thickness and inhibits 45Ca2+ uptake by a subcellular fraction of eggshell gland mucosa of the domestic fowl.

1. Administration of furosemide to egg-laying domestic fowl (single p.o. dose 100 mg/bird) caused a decrease in the thickness of the shell of eggs laid the next day. 2. Furosemide administration in vivo caused a 37% decrease in the uptake of 45Ca2+ by a subcellular fraction of the eggshell gland mucosa (mainly composed of cell fragments and plasma membranes). 3. Furosemide treatment did not affect calcium concentrations in plasma or shell gland fluid but did cause a significant increase in the calcium concentration in shell gland mucosa. 4. It is concluded that the eggshell-thinning effect of furosemide is localized to an inhibitory effect on plasma membrane calcium transport in the eggshell gland mucosa. 5. These findings are discussed and compared with the effects of other drugs and toxic substances known to influence eggshell formation in birds.

Animals↗
PubMed1991

Effects of furosemide on ponies with recurrent airway obstruction.

The effect of aerosol and intravenous administrations of furosemide was examined in ponies with recurrent obstructive pulmonary disease, commonly called 'heaves'. This recurrent airway disease bears many similarities to human asthma. Six ponies with the disease (principal animals) were studied during clinical remission and during an acute attack of airway obstruction precipitated by stabling and feeding dusty hay. Six control animals were also studied. Furosemide (1.0 mg/kg) or vehicle was administered by aerosol in the first study, and intravenously in a second study. In principal ponies with airway obstruction, furosemide administration significantly decreased pulmonary resistance and increased dynamic compliance, but had no effect on PaO2 or PaCO2. The time course and magnitude of lung function changes were similar following aerosol or intravenous drug administration. Vehicle was without effect in both groups of animals at all time periods and furosemide had no effect in controls or in principals in clinical remission.

Aerosols↗
PubMed2026

Comparative effectiveness of torsemide vs furosemide in the management of heart failure patients: Win-ratio reanalysis of the TRANSFORM-HF trial.

BACKGROUND: Loop diuretics are widely used for managing congestion in patients with heart failure (HF). The TRANSFORM-HF trial is a multicenter randomized study that enrolled heart failure patients, comparing a strategy of torsemide vs furosemide. The time-to-event analysis demonstrated neutral effects on all-cause death at 30 months and the composite of all-cause death and first rehospitalization at 12 months. We evaluated whether a hierarchical win-ratio (WR) framework integrating mortality, recurrent hospitalization, and patient-reported health status provides additional interpretive insight. METHODS: This study is a secondary analysis of the pragmatic, multicenter, open-label, randomized TRANSFORM-HF trial, conducted across 60 US hospitals that randomized 2,859 patients hospitalized with HF to torsemide or furosemide. The primary 12-month hierarchical composite outcome was defined as (1) all-cause mortality, (2) recurrent all-cause hospitalizations, and (3) lack of improvement in the Kansas City Cardiomyopathy Questionnaire Clinical Summary Score (KCCQ-CSS). The primary statistical method was a WR analysis adjusting covariates via inverse probability weighting. Subgroup analyses evaluated potential heterogeneity across patient demographics and clinical characteristics. RESULTS: In the primary 12-month intention-to-treat analysis, the adjusted WR was 1.07 (95% CI, 0.98-1.16; P = .13), indicating no significant difference between torsemide and furosemide. A supplementary 30-month analysis with extended mortality follow-up yielded a similar estimate (adjusted WR, 1.06; 95% CI, 0.98-1.16; P = .14); hospitalization and KCCQ-CSS components were assessed through 12 months. As-treated sensitivity analyses were consistent with the neutral primary findings. Exploratory subgroup analyses were not adjusted for multiplicity and should be considered hypothesis-generating. CONCLUSIONS: The overall WR comparison between torsemide and furosemide showed no statistically significant difference in the primary 12-month analysis. The WR framework provided an interpretive decomposition across outcome domains but did not establish superiority of either loop diuretic strategy. All findings should be considered exploratory. TRIAL REGISTRATION: ClinicalTrials.gov, NCT03296813, https://clinicaltrials.gov/study/NCT03296813.

Aged↗
PubMed2006

Effects of standard heart failure therapy and concomitant treatment with intravenous furosemide or inotropes (dobutamine, dopamine, and/or milrinone) on renal function and mortality in patients treated with nesiritide.

The safety and efficacy of the concomitant use of intravenous diuretics and positive inotropes with nesiritide have not been well studied. There is also a paucity of data examining whether the type of medical therapy before treatment with nesiritide has an effect on outcomes. Data from 167 patients with heart failure and reduced left ventricular ejection fractions (34 +/- 17%) treated with nesiritide were analyzed retrospectively. Baseline oral medications were continued, diuretic regimens were modified, and nitrates were discontinued. Forty-three patients (26%) received intravenous furosemide with nesiritide. The glomerular filtration rate before and after nesiritide infusion was not different in patients treated with versus without furosemide (0.7 +/- 8.8 vs 0.7 +/- 11.0 ml/min/1.73 m(2), p = 0.71). Change in urine output from before to during nesiritide infusion was greater with concomitant furosemide (41 +/- 57 vs 10 +/- 58 m/hour, p = 0.006). There was no significant difference in survival with furosemide (90% vs 89% at 30 days, 62% vs 57% at 12 months, p = 0.63). Thirty-nine patients (23%) received inotrope support with nesiritide. The glomerular filtration rate tended to improve when inotropes were used with nesiritide (3.3 +/- 13.1 vs -0.1 +/- 9.4, ml/min/1.73 m(2), p = 0.17). No significant changes in serum creatinine or urine output were observed with inotrope use. Survival was not worsened in those receiving inotropes (p = 0.51). Also, there were no significant differences in serum creatinine, glomerular filtration rate, or urine output in patients who continued to receive angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, beta blockers, or digoxin therapy during nesiritide infusion. In conclusion, there were no observed adverse affects of baseline medical therapy, intravenous diuretics, or intravenous inotropes on renal functions or mortality when used in conjunction with nesiritide in the treatment of decompensated chronic heart failure.

Aged↗
PubMed1977

Sodium intake and furosemide administration in hypertensive patients with renal insufficiency.

The effects of various levels of sodium intake and loop diuretic (furosemide) administration upon arterial pressure and renal function were studied in 11 patients with impaired renal function and essential hypertension. The patients were hospitalized in a metabolic ward and continued taking their usual antihypertensive medications. After a stabilization period, all patients followed the following regiments for 5 to 7 days: period I, 20 mEq sodium diet without diuretic administration; period II, 80 mEq sodium diet and furosemide, 80 mg daily; and period III, 200 mEq sodium diet and furosemide, 240 mg daily. Supine diastolic pressure was lower (P is less than 0.05) during period II than during period I and both supine and standing systolic and diastolic pressures were significantly lower in period III than in period I (P is less than 0.01). No significant differences in the renal clearance of inulin were noted between any of the study periods. In patients with essential hypertension and impaired renal function, consumption of a moderate or liberal sodium diet combined with administration of a loop diuretic agent (furosemide) appears to result in better control of arterial pressure without significant changes in renal function than does strict sodium restriction without diuretic administration.

Adult↗
PubMed1998

Usefulness of losartan, captopril, and furosemide in preventing nitrate tolerance and improving control of unstable angina pectoris.

Sixty consecutive normotensive patients with unstable angina pectoris, who were on continuous intravenous isosorbide dinitrate (ISDN) treatment and had not previously received angiotensin II receptor antagonists, angiotensin-converting enzyme (ACE) inhibitors, or diuretics were randomly assigned to treatment groups receiving intravenous ISDN for 72 hours. No additional treatment was given to group A (n = 15). Captopril, in a test dose of 6.25 mg, and followed by 12.5 mg 3 times daily for 24 hours and 25 mg 3 times daily for the next 24 hours, was given to group B (n = 15). The same dose of captopril plus 40 mg of furosemide in the morning were given to group C (n = 15). Losartan, in a single dose of 25 mg/day and increased to 50 mg after 24 hours was given to group D (n = 15). Nitrate tolerance was evaluated at 24-hour intervals at trough levels of each of the drugs by administering intravenous ISDN (1 mg bolus dose every 4 minutes) and recording the total ISDN test dose required to decrease the mean arterial blood pressure by > or =10%. Treatment with continuous ISDN only (group A) induced nitrate tolerance. The ISDN (mean +/- SD) test dose was 3.5 +/- 1.8 mg at baseline, increasing to 4.9 +/- 2.4 mg at 24 hours, and 8.0 +/- 3.0 mg at 48 hours. The addition of increasing doses of captopril to the continuous ISDN treatment (group B) completely prevented nitrate tolerance. Losartan, however, did not attenuate nitrate tolerance at 24 hours and attenuated it only partially at 48 hours. The addition of furosemide to captopril had no further effect on nitrate tolerance. Of 15 patients in group A (ISDN only), 4 (27%) experienced recurrent ischemic events requiring urgent coronary catheterization. No such events were recorded in group B (captopril), but did occur in 1 patient in each of group C (captopril plus furosemide) and D (losartan) (p = 0.083). Thus, the addition of captopril to the ISDN treatment regimen prevented tolerance to nitrates and improved angina control with apparent safety. Losartan also decreased nitrate tolerance, although to a lesser extent, and also improved angina control. The addition of furosemide to captopril conferred no further benefit.

Adult↗