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Plasma and tissue levels of furosemide in dogs and monkeys following single and multiple oral doses.

35S-Furosemide was administered to beagle dogs and rhesus monkeys as an oral solution on a single and a 20 repeated 5 mg/kg/day dosing regimen. In both species, furosemide is rapidly but incompletely absorbed with peak plasma levels being achieved within one hour after dosing. The plasma level versus time profiles do not appear to be significantly altered as a result of the repetitive dosing regimen employed, although the profiles themselves are quite different for the two species studied. Following single oral doses, the observed peak plasma levels achieved in dogs are approximately eight-fold higher than in monkeys. In dogs, oral administration of furosemide results in a biexponential disposition curve while in monkeys the profile appears monoexponential. The major disposition phase in dogs has a half-life or approximately 30 minutes and is followed by a slow elimination phase with a half-life of approximately 7 hours. Only a small percentage of the absorbed dose is affected by the slow disposition phase and consequently accumulation of furosemide on the once-daily dosing regimen is slight. In the monkey studies, the rapid disposition phase was not observed and the slow disposition phase had a half-life of approximately 11 hours. On the repetitive dosing regimen, the monkey appeared to accumulate furosemide to a slightly greater extnet than the dog and showed a lesser degree of fluctuation within a dosing interval. In both species, liver and kidney radioactivity levels were not detectable three days after a single dose although low levels of furosemide and/or metabolites were observed for six days following the last dose of the multiple dosing regimen. At the dosage level and regimen employed, no unusual or "typical" lesions associated with furosemide were found in the dog and monkey tissues examined histopathologically.

Administration, Oral↗

[Differences in furosemide-induced changes of summating potential and endocochlear potential in guinea pigs].

OBJECTIVE: To investigate the physiological properties of summating potential (SP) and to compare the different changes between SP and endocochlear potential (EP) induced by Furosemide in guinea pigs. METHODS: SP in response to clicks with alternative polarities at 105 dB peSPL was recorded from a electrode in the facial nerve canal. EP was measured with a glass microelectrode in the basal turn of the cochlea. SP and EP were observed simultaneously and continuously after injection of Furosemide or the solution of Furosemide-bovine serum albumin injected into the jugular vein of the animal. RESULTS: Before furosemide application, only SP could be recorded with small or without +SP. After furosemide injection, EP declined dramatically followed by reduction of the -SP which quickly vanished, while +SP appeared or the amplitude increased. When EP recovered to a certain level, +SP disappeared or dramatically decreased and then -SP reappeared. The amplitude of -SP increased progressively with EP recovery. Both -SP and EP recovered to the pre-injected level in 60 min after the furosemide application. CONCLUSION: The results suggest that Furosemide induced distinct changes of -SP and +SP, the two components of SP. The changes of -SP amplitude was consistent with that of the EP value, while the changes of +SP amplitude were contrary to that of the EP value.

Animals↗

[Quantitative determination of furosemide in serum and urine by high-performance liquid chromatography with electrochemical detector].

A high-performance liquid chromatographic method using electrochemical detection is described for the determination of furosemide in serum and urine. Serum proteins were precipitated with acetonitrile containing the internal standard and the clear supernatant was separated. Urine was diluted with water to 50 times. Furosemide was chromatographed on a reversed-phase column, 8MBC18 column, using 35% ethanol solution containing 5 mmol/L tetrabutylammonium phosphate (pH 7.50) as the mobile phase (1.0 ml/min) and detected at 0.90 volts. FD-Val-OH synthesized was used as internal standard in the furosemide assay. The retention times for furosemide and internal standard were 10 min and 15 min, respectively. The amount of furosemide was determined by measuring peak height ratio. The detection limit of furosemide was 16 and 9 ng per ml serum and urine respectively. The calibration curve was linear in the range from 0.25 ng/microliters to 5 ng/microliters (serum) and from 0.5 ng/microliters to 10 ng/microliters (urine). The recovery of furosemide was 100.5% (serum) and 100.6% (urine). Coefficient of variation was less than 4.6%.

Chromatography, High Pressure Liquid↗

Renal response to furosemide in conscious rats: effects of acute instrumentation and peripheral sympathectomy.

In order to investigate whether the renal sympathetic nerves contribute to the compensatory Na reabsorption observed during furosemide-induced volume contraction, furosemide was administered as constant i.v. infusion (7.5 mg/kg/h) in trained, chronically instrumented rats with or without guanethidine-induced peripheral sympathectomy. In addition, the effect of acute instrumentation was evaluated by measuring renal function before and after furosemide infusion in control rats recovering from surgery and halothane anesthesia. Lithium clearance was used as a marker for proximal tubular Na reabsorption, and [3H]inulin and [14C]tetraethylammonium were used as markers for the glomerular filtration rate and the effective renal plasma flow, respectively. Control values in chronically instrumented sympathectomized rats did not differ from values obtained in chronically instrumented control rats. In acutely instrumented control rats the control value for effective renal plasma flow was 20% lower than in both chronically instrumented groups; this was associated with increased arterial blood pressure and increased renal vascular resistance. There were no differences in the diuretic or the natriuretic furosemide response between chronically instrumented control and chronically instrumented sympathectomized rats, whereas the diuretic and natriuretic responses were reduced in acutely instrumented control rats. This was due to an accentuation of the initial fall in glomerular filtration rate during furosemide infusion. In control animals, either acutely or chronically instrumented, fractional Li excretion increased from 30% to 50% during furosemide peak response, after which it returned toward control values. In sympathectomized rats, the fractional Li excretion increased from 36% to 70% during furosemide peak response, after which it decreased to a steady-state value of 56%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Results of treatment for severe congestive heart failure with digoxin, furosemide and vasodilating agents].

In 61 patients with class IV (NYHA) of chronic congestive cardiac failure treated for 2 weeks with digoxin (0.290 +/- 0.108 mg/d) and furosemide (13.0 +/- 4.1 mg/d), for 2 weeks with digoxin, furosemide and isosorbide dinitrate (44.5 +/- 9.8 mg/d) or nifedipine (42.0 +/- 12.2 mg/d), for 4 weeks with digoxin, furosemide, isosorbide or nifedipine and captopril (angiotensin converting enzyme inhibitor) (75.1 +/- 24.4 mg/d), and for the last 2 weeks with digoxin, furosemide, isosorbide or nifedipine without captopril, after each stage the clinical state, exercise tolerance and haemodynamic parameters determined echocardiographically were assessed. Ten weeks of treatment by this method caused regression of pulmonary congestion in 80%, oedema in 63.3% and hepatomegaly in 33.3% of the patients. Moreover, 60.7% of the patients returned to class III, 13.1% to class II, and 26.2% remained in class IV (NYHA). In the group treated with digoxin, furosemide, nifedipine with captopril (n = 30) a significant rise was observed of the value of the ejection fraction and cardiac index in relation to the treatment with digoxin and furosemide and the treatment with digoxin, furosemide, nifedipine (p less than 0.05). No drug improved significantly the tolerance of submaximal exercise. During the treatment with captopril no clinical improvement was achieved in 4 cases, and worsening occurred in 3 cases of severe cardiac failure (7 of 61 patients, 11.5%). The obtained results showed that vasodilating drugs are safe in congestive cardiac failure and in many cases of severe failure captopril contributed to rapid clinical and haemodynamic improvement.

Adult↗

The separate modes and sites of action of furosemide and amiloride.

The effect of furosemide and amiloride on the transport of sodium, potassium, hydrogen and bicarbonate ions was studied in microperfusion experiments on the main excretory duct of the submaxillary gland of the rat. Furosemide did not impair transport of Na+, K+ and H+/HCO-3. Amiloride, however, completely abolished Na+ transport. Blockade of Na+ transport was accompanied by abolition of passive K+ secretion, whereas the active components of K+ and HCO-3 secretion were not affected. In urinary excretion studies, amiloride, which is known to block sodium transport selectively, was used in order to assess whether furosemide has a distinct effect that is independent of sodium transport. Oral administration of amiloride caused a selective excretion of Na+ in a more alkaline urine with an extremely low K+ concentration. The injection of furosemide caused a copious diuresis of an isotonic urine, in which excretion of Na+ and K+ was balanced by the excretion of Cl- ions. Combined administration of amiloride and furosemide produced summation of the individual effects of both diuretics, indicating that the two drugs had different sites and modes of action. In the presence of furosemide the kidney no longer responded to antidiuretic hormone, which suggested that the urine concentrating mechanism in Henle's loop was blocked by furosemide.

Amiloride↗

Effect of organ perfusion on renal drug transport. Application to furosemide in the isolated perfused rat kidney.

Angiotensin II was used as a probe to study the effect of changes in perfusate flow rate on the renal clearance parameters of furosemide in the isolated perfused rat kidney. Drug studies were performed in three rats with no angiotensin II present in the perfusate (treatment I) and in three rats with a 2.7 ng/min infusion of angiotensin II into the perfusate (treatment II). Furosemide was introduced into the recirculating perfusate at an initial concentration of 3.5 micrograms/ml and was assayed using HPLC. The protein binding of furosemide in perfusate was determined by equilibrium dialysis. Angiotensin II was found to have a dramatic effect on the renal hemodynamics, resulting in a 42% decrease in perfusate flow, a 27% decrease in GFR, and a 25% increase in filtration fraction. Values for the fractional excretion of glucose were very low and consistent, with or without angiotensin II (3.0-3.5%). Although the fraction unbound of furosemide was unchanged between treatments (0.770 for treatment I vs. 0.695% for treatment II), the renal and secretion clearances of furosemide were reduced by about 30% in the presence of angiotensin II. However, if the renal clearance (CLr) was corrected for free fraction (fu) and glomerular filtration rate (GFR) [ER = CLr/(fu.GFR)], there was no difference between the excretion ratio (ER) values of furosemide after the two treatments (29.0 for treatment I vs. 29.6 for treatment II). These results imply that the altered clearance parameters of furosemide are more likely the consequence of a reduction in functional nephron mass rather than a change in intrinsic secretory transport per unit mass of nephron.

Angiotensin II↗

Bilirubin displaces furosemide from serum protein: the effect is greater in newborn infants than adult subjects.

The protein binding of furosemide was studied in the serum from 7 umbilical cords and 7 healthy adult subjects in presence or absence of bilirubin. In cord serum, the unbound fraction of furosemide (mean +/- SD) was 2.32 +/- 0.14 (control), 2.94 +/- 0.26 (200 microM bilirubin) (p less than 0.001) and 3.52 +/- 0.38 (400 microM bilirubin) (p less than 0.001). Percent increase (mean +/- SD) of the unbound furosemide was 22 +/- 11 and 51 +/- 12 after 200 and 400 microM bilirubin, respectively. In adult serum, the unbound fraction of furosemide was 1.69 +/- 0.21 (control), 1.93 +/- 0.24 (200 microM bilirubin) and 2.15 +/- 0.38 (400 microM bilirubin). Percent increase of the unbound fraction was 14 +/- 8 and 28 +/- 16 after 200 and 400 microM bilirubin, respectively. Binding of furosemide was also studied in 5 cord and adult serum specimens previously dialysed for 18 h at 4 degrees C. Unbound furosemide in dialyzed serum was 1.39 +/- 0.05 (cord) and 1.25 +/- 0.04 (adult). Cord serum contains dialyzable compounds that enhance the unbound fraction of furosemide. Displacement effect of bilirubin was unchanged by dialysis and it was significantly higher in cord than adult serum. The different displacing effect of bilirubin might suggest the presence of qualitatively different albumin in cord serum.

Adult↗

Dose dependency of furosemide-induced sodium excretion.

Intravenous furosemide doses ranging from 5 to 120 mg were given to healthy young volunteers with and without individualized active rehydration with a sodium chloride solution. Sodium excretion rates and fractional sodium excretions (FENa) percentages were correlated significantly with dose and with urinary excretion rates of furosemide. The ED50 was below 5 mg and no additional natriuretic effect was seen above 40 mg. The efficiency (FENa percentage per microgram of furosemide excreted per minute during a certain clearance period) was dependent on hydration and on time. For the period 15 to 30 min a significant linear relationship between furosemide dose and the reciprocal of the efficiency indicated a higher efficiency for lower doses and a theoretical maximal value of FENa of 0.4% per micrograms of furosemide excreted per minute. A relative value for a dose-dependent efficiency reduction was calculated for each dose. The ED50 for dose-dependent efficiency reduction was about 12 mg i.v. Simultaneous measurements of lithium clearance indicated a proximal site of action for furosemide which was saturated at furosemide excretion rates above 50 micrograms/minute. For the major, distal, site of action no maximal value was demonstrated. It is concluded that a wanted balance between a strong natriuretic effect and weak sodium retaining mechanism not necessarily is achieved by a high dose and that information concerning that problem must be obtained from studies in relevant patient groups.

Adult↗

Chronopharmacological study of furosemide in human subjects.

The present study was undertaken to determine whether the diuretic effects of furosemide depend on the administration time or not. After furosemide 20 mg or a placebo was administered intravenously in 12 human subjects at 09h00 or at 21h00, urine volume and urinary excretion of sodium, chloride and furosemide were determined for 3 h. There were no significant differences in the amount of urine, or of urinary excretion of sodium and chloride between when a placebo was given at 09h00 and when it was given at 21h00. When furosemide was administered at 21h00, the urine volume and urinary excretion of sodium, chloride and furosemide during the first 60 min were significantly greater than those, when the drug was administered at 09h00. There was a marked correlation between the urinary output of furosmeide and the urine volume, urinary sodium and urinary chloride. These results suggest that the diuretic effects of furosemide vary with the time of administration and the observed variations are mainly dependent on the amount of furosemide secreted into urine.

Adult↗

[Blocking effect of furosemide on the chloride permeability of mollusk neuron membranes induced by acetylcholine and gamma-aminobutyric acid].

Furosemide (2.10(-4) to 1.10(-3) g/ml) was shown to prevent the increase of chloride conductance induced in isolated neurons of freshwater mollusc Planorbarius corneus by ionophoretic application of acetylcholine, suberyldicholine or gamma-aminobutyric acid. Furosemide caused no shift in the reversal potential of the chloride-dependent responses if the experiments were carried out employing microelectrode filled with potassium sulphate. When potassium chloride-filled microelectrodes were used, the reversal potential became less negative in the presence of furosemide. This effect seems to be due to the blocking of the active transport of chloride by furosemide. Neither sodium-dependent, nor potassium-dependent responses induced by cholinoreceptor activation were influenced by furosemide. Furosemide was found to diminish both the amplitude and the rate of chloride-dependent responses. The lack of selectivity with respect to acetylcholine or gamma-aminobutyric acid suggests that furosemide blocks the chloride channels of chemoceptive membrane which are probably common to acetylcholine and gamma-aminobutyric acid and does not affect their receptors.

Acetylcholine↗

Role of prostaglandins in the hemodynamic and tubular effects of furosemide.

Loop diuretics, of which furosemide is a prototype, have physiological actions over and above their natriuretic effects to increase renal blood flow, cause renin release, and increase peripheral venous capacitance. The three criteria necessary to show that prostaglandins (PGs) are involved in the action of furosemide include: 1) drug administration should stimulate PG production; 2) infusion of PGs or their precursors should mimic the effect of the drug; and 3) inhibition of PG synthesis must alter the physiological response of the drug. Furosemide administration is associated with an increase in the urinary excretion of all the renal PGs, which suggests that the drug stimulates the deesterification of arachidonic acid from cellular phospholipids. In addition, intrarenal administration of arachidonic acid, PGI2, or PGE2 to experimental animals causes renal vasodilation and renin release, which suggests that PGs can mediate the renovascular and renin-releasing effects of furosemide. Finally, cyclooxygenase inhibitors like indomethacin can block the renal vasodilation, the renin release, and the increase in venous capacitance caused by furosemide administration. The above findings provide a firm basis for the hypothesis that the extradiuretic effects of furosemide to increase renal blood flow, cause renin release, and increase peripheral venous capacitance are mediated by the PG system. Less conclusive are data linking PGs to the renal tubular effects of furosemide and other loop diuretics.

Animals↗

Response of peripheral plasma renin activity (PRA) to furosemide stimulation; reduction of the renal parenchyma as a limiting factor.

The authors examined 34 patients with arterial hypertension, whose glomerular filtration rate ranged from normal to renal failure. The peripheral plasma renin activity (PRA) values were determined before and 30 and 90 min after injecting furosemide. In 17 patients with chronic renal failure treated by haemodialysis and with arterial hypertension, PRA was likewise determined before and after injecting furosemide. In 18 patients, including 13 from this latter group, PRA was determined before and after dialysis. It was found that: 1) In the group of non-dialysed patients, mean PRA rose significantly after the injection of furosemide. In dialysed patients it was not affected either by furosemide or by dialysis. 2) In non-dialysed patients, the ability of PRA to be stimulated by furosemide fell together with inulin clearance (Cin) in a significant hyperbolic relationship. 3) PRA changes in dialysed patients were indistinct and variable. A significant direct correlation was found between the absolute change in PRA after furosemide and after dialysis. These findings show that the degree of damage to the renal parenchyma must be taken into account when evaluating the response of PRA to furosemide stimulation.

Adult↗

[Furosemide effects in patients with chronic renal insufficiency].

In 8 patients with a slight restriction of the renal function (serum creatinine 150-300 mumol/l), 10 patients with a severe restriction of the renal function (serum creatinine greater than 300-1,200 mumol/l) and in 10 control persons with intact renal function on 2 subsequent days after 40 and 80 mg furosemide the pharmacokinetic data were calculated intravenously from the course of the serum concentration and the renale excretion as well as pharmacodynamic parameters. In comparison to the control persons in patients with creatinine values of more than 200 mumol/l still 4 hours after intravenous injection furosemide could be proved in the serum. According to this the excretion of the unchanged furosemide was clearly decreased in the 24-hour-urine. In decreased renal clearance of furosemide the elimination half-life period was prolonged. In all three groups of patients the diuretic effect of furosemide was very distinctly marked in the first four hours after injection of 40 mg, a doubling of the dose did not increase this effect. Only in the first four hours also an increased excretion of sodium, chloride and calcium occurred; in the 24-hour-collection period no differences between the three groups were the result. The excretion of creatinine and urea-N in the urine was not influenced by furosemide. Thus also in the chronic renal insufficiency there is the indication of the furosemide therapy only then, when the extracellular space or the intravasal volume are enlarged. As individual dose 40 mg are recommended intravenously.

Blood Urea Nitrogen↗

Diuretic effect and duration of action of a single intravenous dose of furosemide in uremia and myocardial infarction.

Furosemide was given in a single dose of 80 mg to 10 normal subjects, 10 uremic and 6 subjects with uncomplicated myocardial infarction. Furosemide overall effects and rates of urine flow, sodium and potassium excretion in different pathophysiological states were compared. During 24 hours furosemide resulted in a two-fold increase in urine flow in both normal and myocardial infarction subjects when compared to 1.4 in uremic patients. Furosemide produced nearly a two-fold increase in 24 hours. Na excretion was in all the three groups studied. K excretion in 24 hours was higher in myocardial infarction patients than uremics and normals, but the difference was not significant (p less than 0.05). Rate-time plot for urine, Na or K excretion showed that the decline was slower in uremic or myocardial infarction patients than in normal subjects. The smaller decay constants for effect in both uremic and myocardial infarction subjects were indicative of longer duration of action of furosemide in these patients. No correlation was observed between overall Na or K excretion after furosemide and creatinine clearance. Changes in renal function or renal hemodynamics produced decreased but prolonged effects of furosemide and eventually the overall diuretic effect of the drug was slightly altered.

Adolescent↗

Pharmacodynamic and pharmacokinetic study of a slow-release formulation of furosemide in man.

A slow-release formulation of 40 mg furosemide as capsules (Eutensin) was investigated for its pharmacokinetic and pharmacodynamic properties in comparison with conventional tablets containing 40 mg furosemide (Lasix) in a single-blind clinical pharmacological trial in 6 healthy subjects. The following results were obtained: 1. The AUC0-24 after the administration of slow-release (SR) furosemide was about 42% of that after furosemide tablets. 2. Urine volume and urinary excretion of Na and Cl were significantly greater after furosemide tablets than after SR furosemide during the first 10 h after administration. No significant difference was observed between the two formulations in the urinary excretion of K, creatinine and uric acid. No significant difference was noted in every tested pharmacodynamic parameter during the cumulative 24 h after administration. It was concluded that SR furosemide may be used in the treatment of hypertension due to its characteristics of a slow-release diuretic feature, delayed peak blood concentration, delayed maximum diuretic effect and prolonged duration of action.

Adult↗

[Furosemide and metolazone: a highly effective diuretic combination].

The natriuretic and diuretic effects of combined treatment with furosemide and metolazone have been studied quantitatively. 15 hospitalized patients with severe fluid retention who showed no reduction of body weight despite treatment with furosemide received metolazone in addition for 3 days. 11 patients had biventricular heart failure with edema, and 4 had cirrhosis of the liver with ascites. Following the addition of metolazone at a starting dose of 2.5 mg/d, a highly significant increase in diuresis and natriuresis, with a corresponding reduction in body weight, was seen in all patients pretreated with a daily dose of 40-370 mg furosemide (mean 122 mg/d). On the first day of this combined treatment the mean sodium excretion increased from 131 to 303 mval/d (2 p less than 0.01) and the mean urine volume increased from 1677 to 2940 ml/d (2 p less than 0.01). The mean reduction in body weight was 6.1 kg (2 p less than 0.001) within 7 days of continuous treatment. Even at low doses metolazone significantly potentiates the diuretic effects of furosemide and therefore simplifies the treatment of fluid retention. High doses of furosemide can be avoided in many cases, a factor of particular advantage in ambulatory long term therapy and in patients with decreased kidney function. It may also lower the cost of the therapy. In 3 patients the furosemide dose had to be lowered after metolazone was started, to avoid an excessive negative fluid balance. These cases clearly demonstrate the importance of daily checks on the patient's body weight after starting combined therapy with furosemide and metolazone.

Ascites↗

Furosemide disposition in cirrhotic patients.

Furosemide disposition in 7 cirrhotic subjects and 4 age-matched healthy controls was studied to determine the contribution of differences in pharmacokinetics to the decreased responsiveness observed in cirrhotics. Subjects were given 80 mg of furosemide orally and intravenously on separate occasions, and plasma and urine samples were collected and analyzed for furosemide by high performance liquid chromatography. The half-life of furosemide was 74% greater in the cirrhotic subjects, the result of a smaller increase in volume of distribution (30%) and a decrease in total plasma clearance (15%). The change in plasma clearance was due entirely to a change in nonrenal clearance, since renal clearance was very similar in both groups. The fraction of furosemide not bound to plasma proteins increased by 48%. Furosemide bioavailability was the same in cirrhotic subjects and controls. Consistent with other reports, there was considerable intersubject variability in all of the measured and computed parameters. The results show that differences in disposition play little, if any, role in the decreased renal responsiveness to furosemide.

Administration, Oral↗