Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FUROSEMIDE”

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

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

At least 1,153 records · Page 64Linked to original sources
PubMed1984

[Mechanism of the decrease in intracranial pressure as affected by furosemide].

The correlation was established between the increase in diuresis and natriuresis and fall of CSF pressure after intravenous injection of 10 mg/kg furosemide into dogs. Osmolarity and ion concentration in the serum and CSF did not change in these experiments. In nephrectomized dogs, furosemide did not changes CSF pressure. Furosemide dehydrated brain with traumatic edema, reduced brain Fe content probably due to diminishing brain blood content. The mechanism of intracranial pressure fall after furosemide injection can be explained by acute excretion of a large volume of fluid by the kidneys, leading to a decrease in the blood content of the skull cavity.

Animals↗
PubMed1978

Effects of ethacrynic acid and furosemide on respiration of isolated kidney tubules: the role of ion transport and the source of metabolic energy.

In order to investigate the mechanism of action of ethacrynic acid and furosemide, experiments were designed to determine whether these drugs directly inhibit active transport or energy metabolism. The effects of these diuretics on the respiration of tubule suspensions isolated from renal cortex (of rats and rabbits) and outer medulla (of rabbits) were measured. The respiration of tubules prepared from renal outer medulla was stimulated by the presence of chloride in the incubation medium, whereas the respiration of cortical tubules was unaffected by chloride. Both ethacrynic acid and furosemide produced the greatest inhibition of respiration on tubules from outer medulla suspended in chloride-containing media; this result suggests that the diuretics directly inhibit chloride transport. The source of metabolic energy for ion transport was varied by using substrates which donate electrons to the respiratory chain at different phosphorylation sites. Both ethacrynic acid and furosemide inhibit respiration supported by beta-hydroxybutyrate, but there was little or no inhibition of respiration with succinate or tetramethylphenylenediamine ascorbate. Similarly, ouabain inhibited respiration with beta-hydroxybutyrate, but not with the other substrates. Therefore, both diuretics inhibited respiration in a fashion similar to ouabain. It is concluded from both types of experiments that ethacrynic acid and furosemide may directly inhibit active chloride transport.

Animals↗
PubMed1983

Pharmacodynamics of the diuretic effects of aminophylline and acetazolamide alone and combined with furosemide in normal subjects.

The current study was performed in normal subjects to assess the mechanism of the natriuretic effects of aminophylline, to confirm the effect of acetazolamide on the proximal tubule and to assess the pharmacodynamics of the combination of aminophylline and of acetazolamide with furosemide. None of these agents or their combination affected renal hemodynamics. Aminophylline inhibited solute reabsorption at the diluting segment manifested by a 15% decrease in free water clearance relative to solute delivery (P less than .001). In addition, it decreased solute reabsorption in the proximal nephron. Acetazolamide affected only the proximal tubule. The combination of either aminophylline or of acetazolamide with furosemide was little different from furosemide alone. Analysis of dose-response curves to furosemide revealed a minor additive, i.e., parallel upward shift, of the dose-response curves with both combinations.

Acetazolamide↗
PubMed1984

Clinical investigations on the pharmacology of azosemide (SK-110) in comparison with furosemide in healthy volunteers.

In this study, 60 mg of Azosemide and 40 mg of Furosemide were each administered to 2 volunteer persons. The daily urine volume after administration of both drugs was almost the same. Azosemide didn't show such rapid diuretic effect as was seen in Furosemide, but Azosemide proved to have a mild diuretic and protracted effect as compared with Furosemide. The influence on a daily urinary and fecal excretion of electrolyte and the decrease of serum electrolytes proved to be the same in administration of either drug. However, in the case of Furosemide, most of the electrolytes were excreted within 3 hours after administration, while Azosemide showed mild and prolonged excretion. The effect of both drugs on serum uric acid was almost the same showing a slightly rising trend.

Adult↗
PubMed1982

Furosemide chronopharmacology.

Twelve healthy males participated in a trial to determine whether furosemide diuresis and its effects on electrolyte excretion patterns, aldosterone concentrations and renin activity are subject to diurnal variations. Six treatments were give: placebo at 07h00, 13h00 and 19h00 and furosemide 40 mg at 07h00, 13h00 and 19h00. Each subject participated in six phases. It was found that the time of administration of furosemide does not affect the effect of the drug on sodium and potassium excretion and diuresis. There is a tendency for furosemide to elevate serum aldosterone levels and renin activity regardless of the time of administration.

Adult↗
PubMed1981

Effect of furosemide on collecting-duct hydrogen ion secretion in the rabbit.

The purpose of this study was to determine the effect of acute furosemide administration on urine acidification. U-B Pco2 was used to assess collecting-duct hydrogen ion secretion in rabbits infused with bicarbonate. Prior to furosemide administration, the U-B Pco2 was virtually zero, indicating very low or absent hydrogen ion secretion in the collecting duct. Intravenous furosemide infusion resulted in a significant increase in the U-B Pco2. This increase could not be attributed to changes in blood Pco2, plasma potassium concentration, or urine phosphate concentration and buffer capacity. Furthermore, the rise in U-B Pco2 was independent of any change in urine bicarbonate concentration. We conclude that furosemide leads to an augmentation of collecting-duct hydrogen ion secretion in the rabbit, perhaps by increasing sodium reabsorption in the collecting duct.

Animals↗
PubMed1983

Role of binding in distribution of furosemide: where is nonrenal clearance?

Furosemide is an acidic drug that binds tightly to anionic binding sites on albumin, but has negligible binding to tissue proteins. As a consequence, it has a low volume of distribution of total drug at steady state (Vdss total), which is less than extracellular fluid volume. With decreases in serum albumin concentration, plasma protein binding decreases, total Vdss increases, and Vdss of free drug decreases in a manner that is quantitatively consistent with no change in tissue binding. The elimination of furosemide is partly by renal clearance of unchanged drug (predominantly because of renal tubule secretion) and partly by nonrenal routes. Glucuronidation appears to occur in extrahepatic sites in dogs and, possibly, humans. Residual nonrenal elimination is not influenced by liver disease but is reduced by probenecid pretreatment and uremia. Furthermore, there is appreciable recovery of 35S-labeled furosemide in feces after i.v. administration without the appearance of 35S in the bile. These observations are consistent with the hypothesis of active secretion of furosemide into the gut. The independent variables of distribution and elimination contribute to determine intersubject variability of plasma concentration-time profiles in health and disease and, therefore, are important in determining the extent and duration of diuretic response.

Furosemide↗
PubMed1983

Determinants of the overall response to furosemide: pharmacokinetics and pharmacodynamics.

After an oral or i.v. dose of furosemide, there is considerable interindividual variability in the amount of unchanged drug delivered into the urine. On the average, approximately half as much reaches the intraluminal site of action with an oral compared with an i.v. dose. However, the natriuretic response to the same dose administered by either route is virtually the same. Similarly, after pretreatment with probenecid, the same total amount of furosemide in urine causes a greater overall response. It has been presumed that this paradox is accounted for by differences in rate of delivery of furosemide to the active site such that after an oral dose or after pretreatment with probenecid, amounts of drug are at the "steep" portion of the dose-response curve for longer periods of time. Our analysis shows that this is not the case. For furosemide, the amount of diuretic delivered into the urine that is maximally efficient (21.5 micrograms/min) is considerably less than the amount causing half-maximal response (69.8 micrograms/min). Oral administration or pretreatment with probenecid maintains drug close to this maximally efficient amount more persistently than does i.v. administration. By so doing, total response to an oral dose approaches that of i.v. dosing despite delivering half the amount of drug to the active site, and after probenecid an i.v. dose causes a greater response than i.v. dosing alone despite delivering the same amount of drug to the active site. These data emphasize the importance of the time course of delivery of drug to the active site as an independent determinant of overall response.

Dose-Response Relationship, Drug↗
PubMed1981

The effect of prostaglandin inhibition on renin release. A comparison of furosemide and low-sodium stimulation tests.

Furosemide administration is considered comparable to sodium restriction and upright posture as a stimulation test of PRA. This view can be questioned if different mechanisms of renin release are involved. Prostaglandins appear to be an important mediator of renin release. Using a prostaglandin antagonist, indomethacin, we attempted to assess the relative role of prostaglandins in the two renin stimulation tests. Eleven healthy volunteers on a high-sodium intake had PRA and PA measured in response to furosemide stimulation before and during indomethacin administration and then in response to sodium restriction combined with upright posture before and during indomethacin. Supine PRA was 0.41 ng/ml/hr on high sodium and 0.19 after indomethacin (p less than 0.05). On low sodium, the supine PRA was 2.07 ng/ml/hr and 0.98 after indomethacin (p less than 0.05). The increase in PRA (delta PRA) was 3.26 ng/ml/hr with furosemide stimulation and 1.23 after indomethacin (p less than 0.025). The PRA was 3.71 ng/ml/hr with low-sodium stimulation and upright posture and 2.53 after indomethacin (NS). PA paralleled PRA except that there was no suppression of supine values with indomethacin. We conclude that prostaglandins mediate baseline renin secretion and renin stimulation in response to furosemide. However, no comparable prostaglandin mediation could be demonstrated during renin stimulation secondary to sodium restriction. The two standard renin stimulation tests appear to involve different mechanisms of renin release.

Adult↗
PubMed1982

Pathophysiology of furosemide ototoxicity.

Furosemide is a very commonly used loop diuretic in current clinical practice. Ototoxicity is a significant side effect which may be transient or permanent. Investigations into the mechanisms of furosemide ototoxicity have used pharmacologic, neurophysiologic, and morphologic methods, but the exact mode of production of ototoxicity is unknown. Aminoglycoside antibiotics potentiate furosemide ototoxicity, but noise trauma apparently does not. Methods of avoiding ototoxicity are suggested including slow continuous infusion rather than bolus injection, use of divided oral dose regimens, and the measurement of blood levels to avoid exceeding 50 mcg/ml of furosemide. If a diuretic response cannot be obtained using the above measures, the substitution of another diuretic such as bumetanide is suggested to maintain the therapeutic response and minimize the ototoxicity.

Aminoglycosides↗
PubMed1982

Furosemide in the intraoperative reduction of intracranial pressure in the patient with subarachnoid hemorrhage.

The effect of furosemide in the intraoperative reduction of intracranial pressure was measured in 25 patients undergoing the operative repair of a ruptured intracranial aneurysm. Seven patients with similar intracranial lesions served as controls. A single bolus of 80 mg of furosemide was administered intravenously after the induction of anesthesia, and sequential measurements were made of intracranial pressure, mean arterial pressure, and arterial blood gases. A mean decrease of intracranial pressure of 56% was measured in the furosemide-treated patients, whereas the control patients demonstrated a mean decline of subarachnoid pressures of 18%. These changes are significant at the P less than 0.005 confidence level, whereas changes in mean arterial pressure, mean arterial pCO2, and base line arterial pCO2 were statistically insignificant. This study suggests that intravenous furosemide is a quick, dependable, and effective mechanism for the intraoperative reduction of intracranial pressure in the postsubarachnoid hemorrhage aneurysm patient.

Adult↗
PubMed1982

Inhibition of calcium absorption in the cortical thick ascending limb of Henle's loop by furosemide.

The effect of luminal furosemide on calcium transport across the cortical thick ascending limb of Henle's loop was studied. Cortical thick ascending limbs were dissected from rabbit kidneys and perfused in vitro. Calcium concentrations in perfused and collected tubule fluids were measured by continuous-flow microcolorimetry. Tubules were perfused at slow flow rates and parathyroid hormone was added to the bathing solution to maximize the difference between perfusate and collectate calcium concentrations. Furosemide simultaneously and reversibly inhibited the lumen-positive transepithelial voltage and calcium absorption. In the presence of furosemide perfusate-minus-collectate calcium concentration difference was smallest under conditions that minimized the residual transepithelial voltage. It was concluded furosemide inhibits calcium absorption in the cortical thick ascending limb of Henle's loop by reducing the lumen-positive transepithelial voltage that drives passive calcium ion transport.

Absorption↗
PubMed1982

Vancomycin in rabbits: pharmacokinetics, extravascular diffusion, renal excretion and interactions with furosemide.

The pharmacokinetics, renal excretion, protein binding and extravascular diffusion of vancomycin in rabbits were studied. The effects of furosemide on these different parameters also were investigated. We observed a T 1/2 of 55 min and protein binding of 65% as determined in vitro by equilibrium dialysis. Vancomycin appeared to be secreted by renal tubules (fractional excretion: 177 +/- 44%). In vitro, furosemide (5 micrograms/ml) slightly decreased the vancomycin protein binding (from 65 to 57%). Furosemide significantly increased the renal excretion of vancomycin, through a tubular process without any effect on the filtered load. Vancomycin appeared slowly and at low concentrations in the extravascular fluid. The extravascular concentrations were higher when the antibiotic was administered by a 6-hr continuous infusion than when given by a 20-min infusion of the same dose. Our results suggested that the in vivo antibacterial effect to vancomycin could be enhanced by prolonged infusion. Also, it was demonstrated that furosemide has only a small effect on the kinetics of vancomycin.

Animals↗
PubMed1982

[Effects of furosemide on renal functions in prematures (author's transl)].

Renal effects of Furosemide were examined during the first 2-4 days of life in preterm infants suffering from respiratory distress syndrome. Administration of the drug was followed by a sevenfold increase of diuresis. This latter was a result of both a rise in sodium excretion and glomerular filtration. The possible mechanism of Furosemide induced alteration in the glomerular filtration is discussed. Furosemide also altered the hydrogen-ion excretion: both the urinary bicarbonate, the titratable acidity and the ammonium excretion increased. There was a significant rise in the net acid excretion and hydrogen clearance too. It has been found that besides its diuretic effect Furosemide might play a role in the renal hydrogen elimination.

Acid-Base Equilibrium↗
PubMed1982

Comparison of azosemide and furosemide in ascitic patients without and during administration of spironolactone.

Clinical, pharmacodynamic, and renal effects of a new diuretic, azosemide, were studied and compared with those of furosemide. Graded single intravenous (100-1600 mg) or peroral (100-400 mg) doses were administered to six patients with ascites due to liver cirrhosis without and during basic treatment with spironolactone. A standard peroral dose (160 mg) of both diuretics was found to have similar effectiveness. There was no difference in the time-course of action as determined on the basis of 24-h urine volume, sodium excretion, and osmolal clearance in four patients during basic treatment with spironolactone. However, azosemide appeared to be more effective than furosemide in those patients in whom a dose-response curve was established. Unlike furosemide, azosemide was much more effective when given intravenously than orally. Our study confirmed that azosemide is a "loop diuretic" with renal sites of action similar to those of furosemide. However, it has a higher efficiency, probably due to the steeper dose-response relationship.

Administration, Oral↗
PubMed1981

[Pharmacokinetic interference between furosemide and cephalosporins].

The effect of furosemid was studied on rats in comparison to that of etamid with respect to circulation in the body of some cephalosporins, such as cephalotin, cephaloridin, cephazolin, cephacetrile, cephapirin, cefradin and cefalexin. Furosemid and etamid were administered to the rats intraperitoneally in a dose of 100 mg/kg 30 minutes before exposure to the cephalosporins. Cefalexin was administered intragastrically in a dose of 100 mg/kg and the other cephalosporins were administered intramuscularly in a dose of 20 mg/kg. It was found that furosemid increased the blood levels of all cephalosporins in the rats and especially those of cephaloridine and cephacetrile, the levels being increased 5-6 times. The effect of etamid was analogous but less pronounced. Furosemid significantly decreased the renal excretion of some cephalosporins, i.e. cephaloridine, cephalotin, cephacetrile and cephazolin and had an insignificant effect on renal excretion of the other antibiotics. Etamid did not inhibit renal excretion of the cephalosporins.

Animals↗
PubMed1978

Effect of furosemide on mesenteric blood flow in the dog.

Diuretic therapy has been implicated as a possible inciting factor in nonocclusive mesenteric infarction. In view of this possibility, the effect of furosemide on superior mesenteric arterial blood flow (MBF) was investigated using electromagnetic flow probes in pentobarbital anesthetized dogs. After administration of furosemide, 1 mg/kg iv, MBF decreased by 44%. To assess the role of extracellular volume depletion induced by the diuresis in reducing MBF, volume depletion was prevented by infusing isotonic saline at a rate matching urine flow. In these experiments, MBF was not decreased by furosemide. Thus furosemide induces a marked decrease in mesenteric blood flow and this hemodynamic action involves a mechanism that is dependent upon the volume depletion induced by the drug.

Animals↗
PubMed1995

Effects of furosemide, exercise, and atropine on tracheal mucus transport rate in horses.

Effects of furosemide, exercise, and atropine on tracheal mucus transport rate (TMTR) in horses were investigated. Atropine (0.02 mg/kg of body weight) administered IV or by aerosolization significantly (P < 0.05) decreased TMTR at 60, but not at 30 minutes after its administration in standing horses. Furosemide (1.10 mg/kg, IV) did not have any significant effect on TMTR when measured at 2 or 4 hours after its administration in standing horses. Exercise alone or furosemide (1.10 mg/kg, IV) administration followed 4 hours later by exercise did not alter TMTR, compared with values for standing control or exercised horses administered saline solution. Atropine (0.02 mg/kg, IV) administered after exercise significantly (P < 0.05) decreased TMTR, compared with values for no exercise standing controls, for exercise after administration of saline solution, and for furosemide and exercise.

Aerosols↗