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PubMed1982

Effect of cimetidine on the absorption and efficacy of orally administered furosemide.

In six normal subjects who received single oral doses of 400 mg cimetidine and 40 mg furosemide, the area under the furosemide plasma concentration-time curve was increased in two subjects by less than 50%, in two by 59% and 75%, and remained unchanged in two: overall the mean increase of approximately one-third achieved statistical significance. This increase was not accompanied by any significant effects on other pharmacokinetic parameters or urine volume, sodium or potassium excretion during the 8 h subsequent to drug administration. Furosemide produced no effects on cimetidine pharmacokinetics. In another group of subjects, administration of 1.0 g cimetidine/day in divided doses before dosing with 40 mg furosemide produced no significant effects on furosemide plasma levels or in its effects on urinary water and electrolyte excretion.

Absorption↗

PubMed1982

[Effects of ouabain and furosemide on right ventricular function, pulmonary and renal circulation ].

Digitalis glycosides are often used in the treatment of cor pulmonale. However, several investigators have shown that these drugs produce an increase of pulmonary vascular resistance. Combination of other drugs which could reduce this unfavorable effects is to be explored. The purpose of this study is to observe the effects of ouabain on the systemic, pulmonary and renal hemodynamics and right ventricular function with special emphasis on modification of its effects in combination with furosemide. Normal open-chest dogs anesthetized with pentobarbital sodium were used under artificial ventilation. Isolated dog lung lobes were also examined in which perfusion was maintained with heparinized autologous blood at a constant flow rate by a pulsatile pump. In normal dogs, intravenous ouabain administration (0.03 mg/kg) resulted in rise of systemic, pulmonary and renal vascular resistance. However, furosemide (5 mg/kg), when given 3 minutes after ouabain administration, suppressed the vasoconstrictive effect of ouabain. Right ventricular tension (measured by strain gauge arch) was increased after ouabain administration, but this increase was not altered by the combination with furosemide. In the isolated lung lobe, ventilated with normal alveolar gas (14.7% O2, 5.4% CO2) and hypoxic gas (5% O2, 5.4% CO2), ouabain (0.48 mg) caused significant rise of pulmonary inflow pressure (P less than 0.05) which was suppressed significantly by furosemide administration (40 mg) given 3 minutes before and after ouabain administration (P less than 0.05). These results suggest that furosemide may be used rationally with ouabain, because of its effects to eliminate the pulmonary vasoconstriction caused by ouabain and to preserve its positive intropic action.

Animals↗

PubMedDate not supplied

The effect of furosemide on renal function in open heart surgery.

The effect of furosemide on renal function in patients undergoing open heart surgery was investigated, using creatinine clearance, urine flow, sodium and potassium excretion as the parameters. The effect of furosemide (2 mg/kg i.v.) on blood flow in arteria renalis and the tissue oxygen tension of the renal cortex and medulla were also investigated experimentally in six dogs. The flow was measured with an electromagnetic flowmeter and the tissue oxygen tension with IBC tissue oxygen electrodes. Prolongation of the perfusion time to more than 60 minutes resulted in a decline of creatinine clearance to appr. 50% of the initial level. Prophylactic furosemide given prior to the perfusion brought down the creatinine clearance to 64% of the initial level. Furosemide, administered either prophylactically just before the cardiopulmonary bypass or after urine flow had declined below 0.5 ml/kg/h, had no effect on the potassium balance in the long perfusion group (over 60 minutes), though it clearly increased the negative potassium balance in the short perfusion group (below 60 minutes). In an experimental work on dogs, furosemide was found to elevate the tissue oxygen tension in the renal cortex and and medulla, and slightly to increase the blood flow in arteria renalis.

Acute Kidney Injury↗

PubMed1981

The effect of furosemide on canine bile flow and biliary excretion of ioglycamide during cholangiography.

The effect of furosemide on biliary excretion of ioglycamide and bile flow during experimental cholangiography was studied in cholecystectomized and anaesthetized dogs equipped with a Thomas cannula through which the common bile duct could be cannulated. Ioglycamide infusion was started one hour after cannulation of the common bile duct, the infusion rate being 4 micromol/min/kg. Two hours later, 2 mg/kg furosemide was injected intravenously. After furosemide administration biliary ioglycamide concentration and bile flow remained the same as before the furosemide administration. Our evidence suggests that furosemide has no effect on the biliary excretion of ioglycamide or bile flow during ioglycamide cholangiography on dogs.

Animals↗

PubMed1980

Effect of furosemide on renal function of the newborn piglet.

The effects of development of renal function on the response of newborns to furosemide was evaluated in an animal model, the newborn piglet. Three ages of piglets were used: 5-day-old, 20-day-old, and 50-day-old. Intravenous administration of furosemide (2 mg/kg) produced a prompt natriuresis in all animals. The natriuresis after furosemide was greatest in the older piglets (110 microEq/min for 50-day-old piglets were 210 microEq/min for 5-day-old piglets). However, the fractional sodium excretion at the peak of the response was near 20% in animals in each age group. Neither the time of peak response nor duration of natriuresis was affected by age. Potassium excretion increased after furosemide and remained elevated after both urine flow and sodium excretion had returned to control. The pattern of potassium excretion was identical for each of the three age groups. Thus, while renal maturation does not markedly affect the response to furosemide, both newborns and older piglets continue to excrete relatively large amounts of potassium after sodium excretion returns to control.

Aging↗

PubMed1978

[Effect of furosemide on ouabain toxicity in guinea pigs (author's transl)].

An attempt was made to study the effect of furosemide on the toxic and lethal dose (LD) of ouabain. Ouabain was infused continuously in guinea pigs anesthetized with urethane. The toxic dose of ouabain was determined by the minimal dose which produced ventricular arrhythmias. The LD of ouabain was 300.8 +/- 13.8 microgram/kg (mean +/- SE) in control guinea pigs. When furosemide was administered in a dose of 2 mg/kg i.v. prior to ouabain, this was significantly decreased to 225.2 +/- 14.1 microgram/kg (P less than 0.01). Furosemide-treated guinea pigs also showed a marked decrease in toxic dose of ouabain. In another series of experiment, the ouabain uptake by the heart and its subcellular fraction were determined by the infusion of 3H-ouabain at a constant rate under the same experimental conditions aforementioned. Approximately 30% decrease in the LD of 3H-ouabain was also observed in the furosemide pretreated guinea pigs. 3H-ouabain concentration in blood, cardiac muscles and microsomal fraction were lower than control group. These findings suggest that potentiation of ouabain toxicity produced by furosemide is not associated with increased cardiac ouabain uptake, but with increased sensitivity at the site of action.

Animals↗

PubMed1993

Heterogeneous blood pressure response to furosemide and captopril in primary aldosteronism.

The hypertension associated with primary aldosteronism (PA) is often regarded as volume dependent/salt-sensitive. However, not all patients sustain an increase in blood pressure upon sodium loading. In order to examine the sodium sensitivity in PA, 21 patients with aldosteronoma were tested for acute hypotensive response to intravenous furosemide and oral captopril. Ten patients having a decrease in mean blood pressure (MBP) exceeding 5% at the second hour after a 20 mg furosemide injection were defined as diuretic-responders (DR), while the remainder were defined as diuretic-non-responders (DN). The DR group had a higher baseline MBP (135 +/- 6 [mean +/- SE] vs 121 +/- 4 mmHg, p < 0.05) and serum sodium concentration (145.7 +/- 1.4 vs 143.0 +/- 0.7 mmol/L, p < 0.05) than the DN group. The extent of natriuresis induced by furosemide was not different between the two subgroups. Following 100 mg of captopril administered orally, the DR group had a smaller change in MBP (%) than the DN group (3.08 +/- 5.14 vs -7.78 +/- 3.37, p < 0.05). According to the different BP responses to furosemide and captopril, we conclude that PA patients may be further divided into DR and DN. The DR group had a good response to diuretics whereas the DN group responded better to converting enzyme inhibitors. This classification of PA in terms of blood pressure response to furosemide may have therapeutic implications.

Adult↗

PubMed1993

Correlation between renin responsiveness to furosemide and antihypertensive effect of captopril in patients with normal-renin essential hypertension.

The relationship between renin responsiveness to furosemide and the antihypertensive effect of captopril in patients with normal-renin essential hypertension were studied in 23 patients including nine men (mean age, 41 years) and 14 women (mean age, 40 years). Those who had an increment of more than 50% in plasma renin activity (PRA) two hours after an intravenous injection of 20 mg furosemide were classified as group A (n = 13) and the others were classified as group B (n = 10). Baseline PRA, plasma aldosterone and mean blood pressure (MBP) were not different between the two groups. Both groups showed no significant difference in natriuresis following furosemide administration. Significant change in MBP was observed after an oral dose of 100 mg captopril within four hours in group A, but not in group B. These data suggest that renin responsiveness to a single intravenous dose of furosemide can be a useful test for predicting the therapeutic response to captopril in patients with normal-renin essential hypertension. The furosemide test had a sensitivity of 75%, a specificity of 64%, a positive predictive value of 69% and a negative predictive value of 70%.

Adult↗

PubMed1994

[Pure red cell aplasia induced by erythromycin and furosemide effects on in vitro erythroid colony forming unit (CFU-E)].

A 84-year-old man was treated with antibiotics including erythromycin and a diuretic (furosemide) because of acute heart failure and pneumonia. During the treatment, he developed moderate anemia (Hb 8.7g/dl). His anemia improved after the treatment. He again developed marked anemia (Hb 6.3g/dl) during the second treatment with erythromycin and furosemide and received blood transfusions. Bone marrow aspiration study revealed severe erythroid hypoplasia (0.2%). He was referred to our hospital, but he was not treated because his hemoglobin levels and reticulocyte count increased (80%) and his bone marrow showed increased erythroblasts (41.5%). His anemia gradually improved without any treatment. We diagnosed the case as drug-induced pure red cell aplasia (PRCA). We cultured bone marrow cells obtained from the present case and four normal healthy volunteers by a plasma clot method to determine the effects of two drugs on the number of erythroid colony forming unit (CFU-E). Furosemide strongly inhibited the CFU-E colony formation in the patient, but the inhibition effect of erythromycin was moderate. Furthermore, CFU-E was markedly suppressed by a combination of erythromycin and furosemide in both patient and control materials. These results indicate that both furosemide and erythromycin were related to the occurrence of PRCA in this patient.

Aged↗

PubMed1993

Effect of furosemide on physiologic variables in exercising horses.

Twelve horses (6 Standardbreds and 6 Thoroughbreds) received IM injections of furosemide (250 mg) or physiologic saline solution and performed standard exercise tests, to assess the effects of furosemide and breed on blood gas values, PCV, plasma lactate concentration, and heart rate during exercise. After furosemide administration, arterial and venous blood pH values were significantly (P < 0.05) increased. Partial pressures of O2 and CO2 in arterial blood and of CO2 in venous blood (PaO2, PaCO2, and PVCO2, respectively) were unaffected by furosemide treatment, whereas venous partial pressures of O2 (PVO2) were significantly (P < 0.05) less during exercise after furosemide treatment, suggesting an increase in oxygen uptake by the exercising muscles or a change in cardiac output. A significant (P < 0.05) difference was found between Thoroughbred and Standardbred values for arterial and venous pH, PaO2, PaCO2, plasma lactate concentration, and heart rate, suggesting that Standardbreds exercised at a relatively higher work rate than did Thoroughbreds.

Animals↗

PubMed1976

[Nitroglycerin, furosemide and ethacrynic acid effect on hemodynamics in rest and during ergometric load in coronary disease patients].

The haemodynamic effects of intravenous injections of furosemide and ethacrynic acid as well as those of peroral administration of nitroglycerin were studied in 32 patients (4-12 weeks after acute myocardial infarction) during rest and exercise. Cardiac output, heart rate and arterial blood pressure showed no significant changes after administration of nitroglycerin, furosemide and ethacrynic acid (fig 3). A few minutes after application of nitroglycerin or furosemide there were significant falls of pulmonary arteria diastolic pressure and right atrial pressure (fig. 1 and 2), whereas no changes were seen after injection of ehtacrynic acid. This initial effect of furosemide as well as the effect of nitroglycerin is primarily of vascular origin, causing an increased peripheral venous capacitance. Ethacrinic acid failed to exhibit any direct vascular effect. Therefore during pulmonary oedema nitroglycerin together with furosemide should be given.

Blood Pressure↗

PubMed1994

Effect of furosemide on plasma atrial natriuretic peptide and aldosterone concentrations and renin activity in running horses.

Effects of furosemide administration on exertion-induced changes in plasma renin activity and plasma concentrations of atrial natriuretic peptide and aldosterone in horses during sustained submaximal exertion were examined. Furosemide (1 mg/kg of body weight) or heparinized saline solution was administered IV to each of 6 mares not conditioned to exercise, either 4 hours or 2 minutes before 60 minutes of sustained submaximal running on a treadmill. Horses ran at a speed that induced heart rate approximately 65% of maximal after saline treatment. After 15 minutes of running, furosemide suppressed the exertion-induced increase in plasma concentrations of atrial natriuretic peptide (mean [95% confidence interval] values of 63.9 [9.9 to 421] pg/ml vs 100 [15.4 to 652] pg/ml after furosemide or saline treatment, respectively), and enhanced the response of plasma renin activity to exertion (18.6 [5.7 to 60.4] ng/ml/h vs 6.0 [1.8 to 19.4] ng/ml/h, respectively). An effect of furosemide on the exertion-induced increase in plasma aldosterone concentration was not detected.

Aldosterone↗

PubMed1994

Furosemide-induced lysosomal enzyme release in mouse kidney in vivo and in vitro.

The loop diuretic, furosemide, which has been known to elicit renin release in vivo as well as in vitro, has also been shown to induce lysosomal enzyme release. After administration of furosemide (10 mg/kg and 300 mg/kg), a significantly increased acid phosphatase activity (1.33 x 10(-4) and 1.73 x 10(-4) vs. 0.23 x 10(-4) U, p < 0.001) was detected in the urine of the drug-treated mice, accompanied by a reduction of the residual enzyme activity in the kidney (5.0% for 10 mg/kg and 18.4%--p < 0.05--for 300 mg/kg dosage). Two marker enzymes, acid phosphatase and beta-D-glucuronidase, were assayed to demonstrate that furosemide also exerts its effect in in vitro systems like renal cortex suspension (corr. coeff.: 0.899 for acid phosphatase and 0.908 for beta-D-glucuronidase, p < 0.001) and isolated lysosomes (corr. coeff.: 0.981 for acid phosphatase and 0.989 for beta-D-glucuronidase, p < 0.001 for both). This action of the drug seems to be different from the well-known furosemide-sensitive inhibition of ion transport systems and may become of clinical relevance for patients receiving high doses of furosemide.

Acid Phosphatase↗

PubMedDate not supplied

Stability-indicating proton nuclear magnetic resonance spectroscopic assay method for furosemide in tablets and injections.

A simple, specific, and accurate proton nuclear magnetic resonance (1H-NMR) spectroscopic method has been developed for the identification and assay of furosemide and its degradation product, 4-chloro-5-sulfamoylanthranilic acid (CSA), in tablets and injections. Dissolution of the sample in D2O-NaOD resulted in a solution yielding the required separation among the resonance signals of furosemide, CSA, and tert-butyl alcohol, the internal standard. The mean +/- SD recovery values of furosemide and CSA from 10 synthetic formulations were 99.6 +/- 0.8 and 98.9 +/- 1.7%, respectively. Commercial tablets (6 lots) and injections (5 lots) of furosemide were assayed by the proposed method and found to contain 53.1-99.8% furosemide and 0.3-45.2% CSA.

Drug Stability↗

PubMed1995

Does furosemide prevent hypertension during perioperative splenectomy in thalassemic children?

Hemodynamic changes of 50 thalassemic children who had splenectomy under general anesthesia were compared to 40 identical patients who, in addition, received intravenous furosemide 1 mg/kg immediate preoperation. During the anesthetic process, both groups showed a significant increase of heart rate, systolic and diastolic blood pressure more than the preanesthetic values. Hemodynamic variables in the furosemide group declined toward normal range on termination of anesthesia, whereas, the other group's variables were still significantly higher than their control. During the first 24 hours postoperatively, 20 per cent of the furosemide group had blood pressure rising higher than 130/90 mmHg, while 18 per cent was observed in the other group. Antihypertensive drugs were given to reduce the blood pressure in both groups. None of the patients in the furosemide group demonstrated any abnormal neurological symptoms, but 3 out of 50 patients in the other group developed convulsion. We, therefore, conclude that circulatory volume reduction with furosemide does not prevent hypertension during perioperative splenectomy in thalassemic children. However, it's role in prevention of neurological abnormalities needs to be further investigated.

Chi-Square Distribution↗

PubMed1977

Questionable value of furosemide in preventing renal failure.

The effects of furosemide on renal function and hemodynamics were evaluated in 54 critically ill surgical patients. Standard clearance techniques were used to measure glomerular filtration rate (GFR), renal plasma flow (RPF), osmolar clearance (COsm), sodium clearance (CNa), and renal blood flow (RBF). RBF distribution to outer cortex, inner cortex-outer medulla, and inner medulla was measured by the radioactive xenon disappearance technique. Furosemide produced a marked rise in urine output, COsm, and CNa; it produced no change in GFR, RPF, RBF, and RBF distribution. Twelve of the 54 patients received furosemide for therapy not related to the study; six patients developed renal failure and five became hypotensive 2 to 10 hours after administration of furosemide. These data demonstrate that furosemide does not protect against renal failure by altering or increasing RBF but may cause renal failure by producing hypovolemia.

Acute Kidney Injury↗

PubMed1996

Renal nerves do not modulate the renal and endocrine responses to furosemide in conscious lambs.

To test the hypothesis that renal sympathetic nerves influence the renal and renin responses to furosemide in conscious newborn animals, experiments were carried out in chronically instrumented lambs with either bilateral renal denervation (denervated, n = 7, age = 13 +/- 3 (SD) days) or intact renal sympathetic nerves (intact, n = 6, age = 13 +/- 4 (SD) days), at least 4 days after surgery. Basal glomerular filtration rate (GFR), urinary flow, and sodium excretion rates were similar in intact and denervated lambs (p > 0.5). A prompt diuretic and natriuretic response and a decrease in GFR occurred after i.v. furosemide (2 mg/kg); these responses were similar in intact and denervated lambs. Basal plasma renin activity (PRA) was not altered by renal denervation. PRA increased 10 min after furosemide (p < 0.001) and remained elevated at 90 min; the response was similar in both groups of lambs. Basal plasma aldosterone levels were elevated in denervated (191 +/- 232 (SD) pg/mL) compared with intact lambs (62 +/- 24 (SD) pg/mL). Plasma aldosterone levels increased after furosemide administration in both groups of animals. These data provide evidence to suggest that renal sympathetic nerves do not appear to modulate the renal and endocrine responses to furosemide, at least at a dose of 2 mg/kg. Our observations also support the premise that early in life, aldosterone counteracts the effects of renal denervation on fluid and electrolyte homeostasis.

Aldosterone↗

PubMed1996

Molecular effects of M17055, furosemide and thiazide on cardiac hypertrophy of spontaneously hypertensive rats.

Although diuretics have been clinically shown to reduce cardiovascular morbidity and mortality, the effects of diuretics on cardiac hypertrophy are poorly understood. In this study, we examined the molecular effects of diuretics on hypertensive cardiac hypertrophy. Spontaneously hypertensive rats (SHR) were given p.o. M17055 (a novel "high ceiling" diuretic) 1.25, 2.5 or 5 mg/kg/day, furosemide 50 mg/kg/day or trichlormethiazide 30 mg/kg/day for 5 weeks. After the treatment, cardiac myosin isoforms were analyzed by gel electrophoresis, and cardiac hypertrophy-related gene expressions were examined by Northern blot analysis. These three diuretics significantly reduced cardiac hypertrophy of SHR. M17055 and furosemide, but not trichlormethiazide, significantly increased the proportion of cardiac V3 myosin of SHR by enhancing the gene expression of beta-myosin heavy chain. On the other hand, trichlormethiazide, but not M17055 or furosemide, suppressed the increased cardiac gene expression of skeletal alpha-actin in SHR. Cardiac collagen type III expression of SHR was decreased only by treatment with M17055. Plasma thyroid hormone levels of SHR were slightly decreased by M17055 and by furosemide and were negatively correlated with cardiac V3 myosin contents. Thus the effects on the gene expression of cardiac contractile proteins and collagen are significantly different among these three types of diuretics, which suggests that these diuretics may have different cardiac actions independent of their diuretic and antihypertensive actions. The increased cardiac V3 myosin induced by M17055 and by furosemide may be partially due to the decreased plasma thyroid hormone.

Animals↗