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PubMed2006

The significance of the furosemide test for predicting ascites control by diuretics in cirrhotics: a comparison with volume expansion and octreotide infusion.

To verify prospectively the usefulness of the furosemide-induced natriuresis test in predicting ascites control by medical treatment, 15 stable cirrhotics (9 male) with ascites were studied. Sodium excretion was measured after this test and after volume expansion with saline associated with intravenous infusion of octreotide; 6 months later, response to medical treatment was rated as good (N=9) or poor (N=6). Patients with poor ascites control had lower sodium excretion with the furosemide-induced natriuresis test (median, 88 vs 201 mmol; P < 0.01). Poor control was observed in four of four patients with sodium excretion < or =125 mmol, and good control in six of six patients with sodium excretion >175 mmol (P < 0.002). Volume expansion was followed by limited natriuresis (median, 20 mmol), in inverse relationship with plasma active renin concentration (P < 0.001). In conclusion, long-term ascites control is well predicted by the furosemide-induced natriuresis test.

Aged↗

PubMed1981

Mechanisms of hemodynamic actions of furosemide: differentiation of vascular and renal effects on blood pressure in functionally anephric hypertensive patients.

To differentiate diuretic and direct cardiocirculatory properties of furosemide for elucidation of the vasodepressor mechanisms of action of the agent in the acute treatment of hypertension, the peripheral vascular effects of intravenous furosemide (3 mg/kg) on supine blood pressure (BP) and forearm hemodynamics in 11 functionally anephric hypertensive patients (creatinine clearance less than 2 ml/min) were studied. BP was recorded by sphygmomanometer and forearm hemodynamics were measured by strain gauge plethysmography. While diastolic BP decreased only 2.7 mm Hg at 30 minutes, forearm blood flow increased 55% (p less than 0.01) mediated by decreased peripheral vascular resistance of 30% (p less than 0.01) at 15 minutes which dissipated by 30 minutes. Systolic BP, indices of venous capacity, weight, hematocrit, serum electrolytes, and plasma renin activity were unchanged. No diuresis occurred. It is concluded that the early hypotensive effect of furosemide depends upon diuresis.

Adult↗

PubMed1991

Furosemide-131I-hippuran renography after angiotensin-converting enzyme inhibition for the diagnosis of renovascular hypertension.

PURPOSE: We have previously demonstrated the greater sensitivity of 131I-hippuran renography than 99mTC-DTPA scintigraphy to diagnose renovascular hypertension (RVH). This study assesses the predictive diagnostic value of furosemide-131I-hippuran renography after angiotensin-converting enzyme (ACE) inhibition in patients with and without RVH. PATIENTS AND METHODS: All patients were investigated at the University of Miami/Jackson Memorial Medical Center. Twenty-eight patients had RVH and 22 did not. Twenty-eight patients had normal or minimally decreased renal function (serum creatinine level 1.5 mg/dL or less) and 22 had renal insufficiency (serum creatinine level 1.8 mg/dL or more). Renography was performed 60 minutes after oral administration of 50 mg captopril or 10 minutes after intravenous injection of 40 micrograms/kg enalaprilat. Forty milligrams of furosemide were administered intravenously 2 minutes after injection of 131I-hippuran. The residual cortical activity (RCA) of 131I-hippuran was measured at 20 minutes. RESULTS: RVH was unlikely when RCA after ACE inhibition was less than 30% of peak cortical activity. Conversely, RVH was present when 131I-hippuran cortical activity steadily increased throughout the test to reach 100% at 20 minutes. In azotemic patients with RCA between 31% and 100%, RVH was differentiated from intrinsic renal disease by obtaining a baseline renogram without ACE inhibition and comparing RCA in that study and RCA after ACE inhibition. If RCA increased (indicating worsening renal function) after ACE inhibition, RVH was likely; whereas, intrinsic renal disease was more likely if RCA remained unchanged or decreased (indicating improved renal function) with ACE inhibition. The test had a specificity of 95% and a sensitivity of 96% in this population. There was a direct correlation between the results of angioplasty or surgery on high blood pressure and the changes in RCA before and after intervention (n = 20). CONCLUSION: Furosemide-131I-hippuran renography with ACE inhibition is highly predictive in identifying patients with RVH.

Adult↗

PubMed1995

Potential route for fetal therapy: intramembranous absorption of intraamniotically injected furosemide.

OBJECTIVE: Our purpose was to determine whether intraamniotically injected furosemide could be absorbed directly into fetal circulation by the ovine intramembranous pathway. STUDY DESIGN: Nine chronically catheterized fetal sheep, five with an intact and four with a surgically ligated esophagus, were studied for 7 hours on 2 consecutive days. Day 1 was a control day in which the fetal parameters of arterial, venous, and amniotic fluid pressures; heart rate; and urine flow were measured continuously. Fetal and maternal blood, amniotic fluid, and fetal urine were sampled for osmolality, electrolytes, blood gases, and pH twice during the first hour and hourly thereafter. On day 2, 15 mg of furosemide was injected into the amniotic cavity after 1 hour and fetuses were monitored in the same fashion as on the control day. RESULTS: On day 2, both intact and ligated fetuses demonstrated a rapid and prolonged increase in urine flow (p < 0.01) compared with control day fetuses. Esophageal ligation decreased, but did not eliminate, the diuresis. Free water clearance increased equally (p < 0.05) in both groups compared with control fetuses. Sodium and chloride excretion increased significantly in intact (sodium 591% +/- 220% and chloride 763% +/- 295%) and ligated fetuses (sodium 234% +/- 70% and chloride 409% +/- 74%) compared with control fetuses. CONCLUSIONS: Diuresis after esophageal ligation demonstrates that furosemide is absorbed by the ovine intramembranous pathway.

Absorption↗

PubMed1990

Diuresis in hemodynamically compromised patients: continuous furosemide infusion.

We have used continuous infusion of furosemide to achieve diuresis in patients who are stable but hemodynamically compromised after heart operations. With a loading dose of 20 mg and a continuous infusion of 4 to 10 mg of furosemide per hour, mean 24-hour urine output was 5.7 L (238 +/- 65 mL/h). Potassium replacement was 115 +/- 20 mmol [115 +/- 20 mEq/L]. Cardiac index, central venous pressure, and diastolic pulmonary artery pressure did not change significantly, even though hemodynamic support was decreased in each patient. Continuous furosemide infusion is a simple, effective, and reliable method to achieve diuresis in select patients.

Adult↗

PubMed1986

Temporal dissociation in the ability of ouabain and furosemide to inhibit K+-transport in rat submandibular salivary gland slices at various postnatal ages.

Slices of glands from 1, 7, 14 and 21-day-old rats were perfused with a physiological salt solution in a lucite chamber; acetylcholine-induced release and uptake of K were compared to that of adult glands, in the absence and presence of the ion-transport inhibitors, ouabain and furosemide. Without inhibitors, peak K efflux from the glands of 1-day-old rats was 50 per cent of that in 7, 14 and 21-day-old rats, and 33 per cent of that in adults. Maximum K+ uptake was 72 per cent of that in 7, 14 and 21-day-old rats and 61 per cent of that in adults. However, K+ uptake was a larger part (78 per cent) of the preceding efflux in glands of 1-day-old rats than in adult glands (43 per cent) or in glands of 7, 14 and 21-day-old rats (55 per cent). Ouabain (10(-3) M) immediately after a 3-min pulse stimulation with 10(-5) M acetylcholine abolished K uptake at all ages. Furosemide (10(-3) M) inhibited K uptake throughout but its effect increased with age. Thus K+ uptake was 21 per cent less than in the absence of inhibitor in slices from 1-day-old rats but 73 per cent less in adult glands. Similar, but smaller, effects were observed when exposure to furosemide followed acetylcholine. Both K efflux and uptake can thus be elicited in rat submandibular glands from the first day of life and the increased response with age correlates with morphological development and with the progressive, postnatal appearance of acinar cell. The large uptake:efflux ratio suggests that a Na, K pump, responsible for a large portion of K+ uptake, is already present and active in the glands of 1-day-old rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1990

The ATPase activity of saponin-treated rat erythrocytes: regulation by monovalent cations, calcium, ouabain, and furosemide.

The ATPase activities were studied in rat erythrocytes permeabilized with saponin. The concentrations of calcium and magnesium ions were varied within the range of 0.1-60 microM and 50-370 microM, respectively, by using EGTA-citrate buffer. The maximal activity of Ca2(+)-ATPase of permeabilized erythrocytes was by one order of magnitude higher, whereas the Ca2(+)-binding affinity was 1.5-2 times higher than that in erythrocyte ghosts washed an isotonic solution containing EGTA. Addition of the hemolysate restored the kinetic parameters of ghost Ca2(+)-ATPase practically completely, whereas in the presence of exogenous calmodulin only part of Ca2(+)-ATPase activity was recovered. Neither calmodulin nor R24571, a highly potent specific inhibitor of calmodulin-dependent reactions, influenced the Ca2(+)-ATPase activity of permeabilized erythrocytes. At Ca2+ concentrations below 0.7 microM, ouabain (0.5-1 mM) activated whereas at higher Ca2+ concentrations it inhibited the Ca2(+)-ATPase activity. Taking this observation into account the Na+/K(+)-ATPase was determined as the difference of between the ATPase activities in the presence of Na+ and K+ and in the presence of K+ alone. At physiological concentration of Mg2+ (370 microM), the addition of 0.3-1 microM Ca2+ increased Na+/K(+)-ATPase activity by 1.5-3-fold. Higher concentrations of this cation inhibited the enzyme. At low Mg2+ concentration (e.g., 50 microM) only Na+/K(+)-ATPase inhibition by Ca2+ was seen. It was found that at [NaCl] less than 20 mM furosemide was increased ouabain-inhibited component of ATPase in Ca2(+)-free media. This activating effect of furosemide was enhanced with a diminution of [Na+] upto 2 mM and did not reach the saturation level unless the 2 mM of drug was used. The activating effect of furosemide on Na+/K(+)-ATPase activity confirmed by experiments in which the ouabain-inhibited component was measured by the 86Rb+ influx into intact erythrocytes.

Adenosine Triphosphatases↗

PubMed1982

The mechanism of renal clearance of cisplatin (cis-dichlorodiammine platinum ii) and its modification by furosemide and probenecid.

When isolated rat kidneys are perfused with 30 microM cisplatin there is net tubular transport of platinum, resulting in excretion of platinum at a rate 125% of the rate attributable to glomerular filtration alone. Probenecid and furosemide are drugs which have been reported to protect against cisplatin nephrotoxicity, by unknown mechanisms. When probenecid 0.3 mM is included in the perfusate net transport of platinum is increased to 200% of that accounted for by glomerular filtration alone. Increasing the concentration of probenecid to 3.0 mM does not significantly further increase the rate of excretion of platinum. The inclusion of furosemide 0.3 mM in the perfusate has no effect on the net tubular transport of platinum. However, at 3.0 mM furosemide causes a decrease in the net platinum transport and only 93% of platinum filtered at the glomerulus appears in the urine. Thin-layer chromatography revealed the presence of at least three platinum compounds in the urine in addition to cisplatin. We conclude that the renal excretion of cisplatin and its transformation products, even in this model system, is a complex process involving glomerular filtration, tubular excretion and tubular reabsorption.

Animals↗

PubMed1985

Furosemide- and bumetanide-sensitive ion transport and volume control in primary astrocyte cultures from rat brain.

K+ and Cl- transport using 42K+ and 36Cl- was studied in primary astrocyte cultures prepared from neonatal rat brains. A component of 42K+ uptake was sensitive to both furosemide and bumetanide with maximum inhibition being obtained at 1 and 0.01 mM concentrations of the inhibitors, respectively. Furosemide and bumetanide also markedly inhibited uptake of 36Cl-. 42K+ uptake in the presence of ouabain was also sensitive to the omission of medium Na+ and Cl-. These results suggest the existence of a K+ + Na+ + Cl- cotransport system in astrocyte cultures which in many cells has been shown to be involved in volume regulation. We studied volume changes using uptake of [14C]3-O- methyl-D-glucose ([14C]3-OMG), and also ion transport, in attached cells in response to exposure to hyper- or hypotonic medium. Exposure to medium made hypertonic with mannitol resulted in shrinkage of the [14C]3-OMG space of the cells, but did not affect 36Cl- content, expressed as nmol/mg protein. Exposure to hypotonic medium led to a marked increase in the [14C]3-OMG space, rapidly followed by a decrease towards control values. After the cells were then exposed to isotonic medium there was an immediate decrease followed by a slower increase in the [14C]3-OMG space. The increase in the [14C]3-OMG space was partially inhibited by 1 mM furosemide.(ABSTRACT TRUNCATED AT 250 WORDS)

3-O-Methylglucose↗

PubMed1989

Increased furosemide-sensitive sodium influx into erythrocytes in non-insulin-dependent diabetes mellitus associated with hypertension.

Our previous study demonstrated increased sodium (Na+) influx into ouabain-treated erythrocytes in diabetic patients with hypertension. The present study was designed to estimate the effect of furosemide on the Na+ influx in non-insulin-dependent diabetes mellitus (NIDDM) with hypertension. Both Na+ influx in the absence of furosemide (total Na+ influx; TNaI) and furosemide-sensitive Na+ influx (FSNaI) were increased in patients with essential hypertension (group 1, n = 22) than those in non-diabetic, normotensive control subjects without family history of hypertension (control group, n = 26, P less than 0.001 and P less than 0.001, respectively). TNaI and FSNaI in diabetic patients without hypertension (group 2, n = 28) were also higher than those in the control group (P less than 0.02 and P less than 0.001, respectively), but no significant differences were found in TNaI or FSNaI between groups 1 and 2. TNaI and FSNaI in diabetic patients with hypertension (group 3, n = 19) were elevated than those in control group (P less than 0.001 and P less than 0.001, respectively), in group 1 (P less than 0.05 and P less than 0.02, respectively) and in group 2 (P less than 0.001 and P less than 0.001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1995

Bioavailability, pharmacokinetics, and pharmacodynamics of torsemide and furosemide in patients with congestive heart failure.

The bioavailability, pharmacokinetics, and pharmacodynamics of torsemide (10 mg orally and intravenously) and furosemide (40 mg orally and 20 mg intravenously) were determined in a randomized crossover clinical trial in 16 patients with compensated congestive heart failure. Torsemide (time to reach maximum concentration [tmax], 1.1 +/- 0.9 hour) was more rapidly absorbed than furosemide (tmax, 2.4 +/- 2.5 hours), the absorption of which was delayed compared with that in healthy volunteers. Bioavailability of torsemide was also greater and less variable than that of furosemide. All four treatments yielded comparable changes from baseline in 24-hour electrolyte excretion. Based on the relationships between sodium excretion rate and fractional sodium and urinary drug excretion rate, response to both diuretic agents at the level of the nephron was decreased compared with previous studies with healthy subjects. Assessment of the clinical relevance, if any, of the difference in the variability of absorption warrants further study.

Administration, Oral↗

PubMed1977

Effect of bumetanide and furosemide on the thick ascending limb of Henle's loop of rabbits and rats perfused in vitro.

Direct effects of bumetanide and furosemide on the thick ascending limb of Henle's loop (TALH) were compared by using the isolated tubules of rabbits and rats perfused in vitro. Both drugs, applied to the lumen, reversibly suppressed the lumen positive potential (PDt) of the rabbit TALH. Bumetanide also suppressed the PDt in the absence of Na+ where the NaCl of the artificial solutions was replaced by choline chloride. The efflux of 36Cl was also reduced by the addition of bumetanide to the perfusate. The dose-response analysis disclosed that bumetanide was 14 times as potent as furosemide. The onset and duration of bumetanide action was significantly longer than that of furosemide. Bumetanide also suppressed the PDt of the rat TALH when it was added to the perfusate.

Animals↗

PubMed1979

Characterization of furosemide-induced activation of the renal prostaglandin system.

A detailed time course of changes in plasma renin activity (PRA), urinary prostaglandin (PG) E2, PGF2 alpha, thromboxane (TX) B2 and sodium excretion rates following furosemide was obtained in 7 women. PRA increased within the first 15 min and remained elevated all through the experiment. PGE2, PGF2 alpha, TXB2 and sodium increased simultaneously, reached a peak between 15 and 45 min after furosemide and declined thereafter. It is concluded that furosemide induces a generalized activation of the renal PG system temporally related to the increase of renin release and natriuresis.

Adult↗

PubMed1981

Evidence for furosemide-sensitive active chloride transport in vascular smooth muscle.

An inhibitor of Cl- transport, furosemide, interfered potently with the 36Cl steady state exchange in rabbit aortic tissue. On long-term incubation with furosemide, [Cl-]i decreased ECl increased, thereby approaching the resting membrane potential of vascular smooth muscle. Electrophysiological microelectrode studies on rabbit pulmonary arteries revealed a hyperpolarization of 5.5 mV in the presence of furosemide. These findings provide evidence for an inwardly directed chloride pump operating in vascular smooth muscle.

Animals↗

PubMed1985

Furosemide during sustained left atrial hypertension in functionally anephric dogs: intravascular and extravascular pulmonary fluid volumes. V.

The response of intravascular (PBV) and extravascular (EVLW) pulmonary fluid volume was examined using double-indicator techniques (thermal-green dye) in 11 open-chest anesthetized dogs during the production of sustained left atrial (LA) hypertension by a LA balloon over a period of 195 min. In 6 of these animals data were also acquired after the intravenous administration of furosemide (1 mg/kg). The renal effects of the diuretic were blocked by tying off the ureters and the vascular supply of both kidneys. Left atrial pressure (N = 11) was abruptly increased from 2.2 +/- 2.1 mm Hg to 30.2 +/- 4.0 mm Hg (P less than 0.01) and maintained at that level for 120 min. Data were obtained prior to pressure elevation, immediately upon pressure elevation, and then every 60 min for a total of 120 min. At that point EVLW had increased (8.1 +/- 0.8 cc/kg at control to 21.7 +/- 2.0 cc/kg at 120 min, P less than 0.001), as had PBV (6.2 +/- 2.1 cc/kg to 9.1 +/- 3.1 cc/kg P less than 0.01). After furosemide injection (N = 6), LA pressure declined (mean peak reduction of approximately 6 mm Hg at 60-75 min, P less than 0.01), aortic and pulmonary arterial pressure both declined (P less than 0.01). However, EVLW remained unchanged, though PBV decreased significantly (peak decrease at 75 min after furosemide administration of 2.0 +/- 0.4 cc/kg, P less than 0.01). In the untreated dogs, EVLW continued to climb (P less than 0.05 vs treated dogs at 75 min postfurosemide).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Effect of furosemide on fully established low pressure pulmonary edema.

It has been shown that furosemide, via nondiuretic vascular effects, reduces pulmonary shunt and lung water during the development of oleic acid permeability edema. We studied this effect in a fully established stable model of oleic acid permeability edema. Sixteen anesthetized mongrel dogs, mechanically ventilated with a FIO2 of 0.5, were studied 24 hr after induction of pulmonary capillary leak by intravenous oleic acid (0.06 cc/kg). After stabilization of pulmonary capillary wedge pressure (PCWP) in the range of 0.5-3 mm Hg, bilateral ureteral ligation was performed. Furosemide (2 mg/kg) was then administered intravenously to eight dogs (treated group). An equivalent volume of saline was given to eight control dogs (control group). Pulmonary artery (PAP) and capillary wedge pressures (PCWP), thermodilution cardiac output (Qt), thermal dye lung water (LW), venous admixture (Qva/Qt), arterial and mixed venous blood gases (PaO2, MVO2) were then measured at hourly intervals for 4 hr. During this period of time, central hemodynamics (PCWP, PAP, Qt) remained stable in both groups. Indices of gas exchange and edema formation (Qva/Qt, LW, PaO2) did not change significantly in either control or treated animals. We conclude that furosemide, previously shown to reduce pulmonary shunt and lung water in the early phase of oleic acid permeability edema, does not have any effect once the pulmonary injury is well-established.

Animals↗

PubMed1985

Effects of furosemide and captopril on submaxillary gland blood flow and arterial pressure.

The effects of furosemide and captopril were studied in nephrectomized rats with and without submaxillary gland. Captopril increased blood flow, but did not modified blood pressure. Furosemide plus captopril decreased significantly blood pressure. These results suggest a release of kallikrein by furosemide and probably a formation of kinin from plasma kininogen. On the other hand, rats sialodectomized showed no alterations in blood pressure in response to both drugs. These data suggest that submaxillary gland kallikrein participates in the mechanism of blood pressure regulation and blood flow of the gland at least in our experimental conditions. Glandular kallikreins are serine proteases which release kinins from substrates called kininogen. They are found in extracts and secretions of all exocrine glands. This proteases have been implicated in the regulation of exocrine glands and kidney blood flow, in water and electrolyte balance, in blood pressure regulation and in the pathogenesis of experimental and clinical hypertension (Carretero et al., 1978; Martinez Seeber et al., 1982). Glandular kallikreins of exocrine glands and kidney are secreted into the exocrine secretions and urine and also into the vascular compartment, where a local blood flow could be affected. According to Gautvik et al. (1980), rat submandibular gland is an organ rich in kallikrein, and significants amounts of the gland enzyme are release into the circulation after stimulation (Orstavik et al., 1982). Hilton and Lewis (1956) first proposed that glandular kallikrein-kinin system in salivary glands regulates vasodilation, probably through the effect of kallikrein on plasma kininogen.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Furosemide magnifies the exercise-induced elevation of plasma vasopressin concentration in horses.

The purpose of this study was to test the hypothesis that furosemide administration before exercise would cause greater increases in plasma arginine vasopressin (AVP) concentration in exercising horses than exercise alone. Six adult, clinically normal, unfit mares underwent three randomly ordered 60 minute standard exercise tests on an equine treadmill to examine the effect of furosemide administration on plasma AVP concentration. In one trial, furosemide (1 mg kg-1) was infused four hours before exercise (FUR-4) and a placebo (10 ml saline) was infused two minutes before exercise; in another trial the placebo was infused four hours before exercise and drug was infused two minutes before exercise (FUR-2); in a third trial a placebo was infused four hours and two minutes before exercise (CON). During the treadmill test each mare ran up a fixed 4 degrees incline for one hour at a speed previously determined to produce a heart rate of 65 per cent of each horse's maximum heart rate. Venous blood samples were collected at rest in the stall, immediately before exercise while standing on the treadmill, and at 15 minute intervals during the treadmill test. Plasma AVP concentration was measured by radioimmunoassay. In the CON trial, plasma AVP concentration increased 561 per cent (P < 0.05) from 6.3 +/- 1.0 pg ml-1 (mean +/- SE) at rest to 38.8 +/- 12.8 pg ml-1 at the end of the 60 minute run. During the FUR-2 trial, AVP increased 1185 per cent (P < 0.05) from 5.9 +/- 1.7 pg ml-1 to 75.8 +/- 17.7 pg ml-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗