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PubMedDate not supplied

[Mechanism of the therapeutic effect of furosemide and mannitol in hemorrhagic shock and developing acute renal insufficiency].

Acute hypotension leads to the development of anuria, almost complete stoppage of the cortical nephron filtration with blood retransfusion failing to restore the upset functions. But against background of preliminary administered diuretics the blood retransfusion renews filtration and restores diuresis. Preliminary administration of diuretics prevents collapse of the proximal tubules, their administration after blood losses increases the tubular pressure and prevents obstruction of the nephron. Under the effect of diuretics the oxygenation of deep-seated segments of the kidney substantially gains in strength due to an increasing renal blood circulation and diminished vasoconstriction. Diuretics increase the oxidative phosphorylation in the cells of the renal epithelium, help augment accumulation of calcium by renal mitochondria and prevent the development of irreversible hypoxic shifts. Combined administration of furosemide and mannitol represents an effective means of prevention and early treatment of acute renal insufficiency.

Acute Kidney Injury↗
PubMed1977

[Depletive treatment of uncompensated liver cirrhosis with high doses of spirolactone only].

In most regimens proposed for the depletive management of cirrhosis of the liver, spirolactone is associated with other diuretics. Treatment of 28 patients with uncompensated forms by means of spirolactone only, using high, protracted doses determined essentially in accordance with the depletion obtained, is described. The disappearance of signs of water retention was gradual and unattended by difficulties. Normalisation of the urinary Na/K ratio preceded the diuretic response; Increased diuresis led to a slight increase in urinary potassium/day. Higher doses were used in patients with lower urinary Na/K ratios. Here a critical diuretic response was only obtained around the 5th day. Transient low blood sodium and chlorine and high blood potassium were noted; the last parameter was not related to the drug dose, nor to changes in Bun; No marked changes in blood uric acid, calcium, ammonium, bilirubin or sugar were observed.

Adult↗
PubMed1993

Diuretics in postinfarction heart failure.

Severe left ventricular failure, as evidenced by radiographic pulmonary edema or raised left ventricular filling pressure, accompanying acute myocardial infarction, carries a high mortality risk. In this situation, the intravenous loop-diuretic furosemide induces a rapid reduction in the raised left ventricular filling pressure due to an immediate and substantial increase in systemic venous compliance accompanied by increasing diuresis. This diuretic-induced venodilatation is probably due to the release of prostaglandins. The transient systemic arterial constriction and small increase in systemic blood pressure that follows intravenous furosemide probably results from the release of renin and subsequent activation of angiotensin. These diuretic induced hemodynamic changes are accompanied by restoration of the vasodilator reflex, which enables the heart to accommodate an acute volume load. Orally administered loop diuretics achieve slower, but similar, directional hemodynamic changes. There is no information on hemodynamic or neuroendocrine dose-response effects of loop diuretics, and there is no information pertaining to the use of other diuretic groups in this situation. The hemodynamic changes induced by furosemide summate with the changes induced by other anti-heart-failure drugs. In this subset of patients with acute myocardial infarction and severe heart failure, the influence of the diuretics on morbidity incidence and mortality risk remains to be measured.

Cardiac Output, Low↗
PubMed1997

[Successful surgical revascularization after 18 hour ischemia below the knee due to complete avulsion of the popliteal artery].

We report the case of a 33-year-old man after knee luxation and disruption of a popliteal artery, which was missed after repositioning at the first clinic. Eighteen hours later complete discontinuity of the popliteal artery was confirmed by arteriography and an immediate reversed, end-to-end auto-venous graft was interposed under general anesthesia with anterior and posterior fasciotomy prior to blood flow restoration. Forced diuresis with a diuretic mixture and balanced fluid intake were used, and the patient was discharged from the intensive care unit on the 10th postoperative day in good condition with normal diuresis.

Acute Kidney Injury↗
PubMed2000

Variability of diuresis renography interpretation due to method of post-diuretic renal pelvic clearance half-time determination.

PURPOSE: We assessed variability in the interpretation of diuresis renography that may result from using different methods of clearance half-time determination. MATERIALS AND METHODS: We reviewed 152 diuresis renography studies performed at diagnosis or during followup of 53 children enrolled in a prospective study assessing the natural history of unilateral neonatal hydronephrosis. Studies were classified as nonobstructive, indeterminate or obstructive using 4 methods of half-time determination. Intermethod correlation and agreement were evaluated. We compared the proportion of nonobstructive, indeterminate and obstructive classifications by each method, and the interpretation of individual studies based on each method. RESULTS: Among methods we noted a high degree of correlation and fair to excellent agreement (Spearman rho = 0.86 to 0.92 and kappa = 0.57 to 0.86, respectively). However, in 27.8% of intermethod comparisons the proportion of studies classified as nonobstructive, indeterminate and obstructive differed significantly (p <0.05). The classification of pelvicaliceal drainage varied by method for all but the most severely dilated systems. In individual studies classification by 1 method was discordant with classification by another in 19% of comparisons. Of the discordant interpretations 97.7% involved nonobstructive versus indeterminate or indeterminate versus obstructive classifications. CONCLUSIONS: Variability in classifying drainage patterns based on half-time requires that practitioners be circumspect when applying this parameter for managing asymptomatic hydronephrosis. It also necessitates the description of quantitative methodology in published series of this important clinical problem.

Diuretics↗
PubMed2006

The role of ultrafiltration in the management of heart failure.

In the United States, 90% of one million annual hospitalizations for heart failure are due to symptoms of volume overload. Hypervolemia contributes to heart failure progression and mortality. Treatment guidelines recommend that therapy for patients with heart failure be aimed at achieving euvolemia. Intravenous loop diuretics induce a rapid diuresis that reduces lung congestion and dyspnea. However, loop diuretics' effectiveness declines with repeated exposure. Unresolved congestion may contribute to high re-hospitalization rates. Furthermore, loop diuretics may be associated with increased morbidity and mortality due to deleterious effects on neurohormonal activation, electrolyte balance, and cardiac and renal function. Ultrafiltration is an alternative method of sodium and water removal, which safely improves hemodynamics in patients with heart failure. Application of this technology has been limited by the need for high flow rates, large extracorporeal blood volumes, and large-bore central venous catheters. A modified ultrafiltration device has overcome these limitations. Ultrafiltration may be a safe and effective alternative to intravenous diuretics in the treatment of decompensated heart failure.

Journal Article↗
PubMed1999

Is the Gauer-Henry reflex important for immersion diuresis in men?

BACKGROUND: This study examines the relationship between the threshold for plasma vasopressin concentration [PVP] responses and diuresis (Gauer-Henry reflex), and tests the hypothesis that water intake would not influence diuresis. METHODS: Eight men (19-25 yr) underwent four treatments: euhydration in air (Eu-air), euhydration in water immersion (Eu-H2O), and with prior 3.6% hypohydration in air (Hypo-air), and hypohydration in immersion (Hypo-H2O). Ad libitum drinking was allowed during the 3-h experimental and 1-h recovery periods. RESULTS: Drinking was greatest during the first 10 min: 3.5 ml x kg(-1) with Hypo-air (450 ml x 3 h(-1)) and only 1.7 ml x kg(-1) (p < 0.05) with Hypo-H2O (235 ml x 3 h(-1)). At 1 h, concomitant [PVP] decreased from a control level of 6.6+/-1.5 to 4.0+/-1 .0 pg x ml(-1) (delta = 2.6 pg x ml(-1), p < 0.05) with Hypo-air, and from 5.9+/-0.6 to 2.3+/-0.2 pg x ml(-1) (delta = 3.6 pg x ml(-1), p < 0.05) with Hypo-H2O. Urine flow was unchanged from control level (<1.0 ml x min(-1)) with Hypo-air, Hypo-H2O, and Eu-air, but increased to 4-5 ml x min(-1) with Eu-H2O. Neither water intake volume nor urine flow was related to the magnitude of [PVP] depression. Regression of Uosm/Posm ratio on [PVP] and urine flow indicated that [PVP] above 2 pg x ml(-1) did not affect urine flow. Thus, ad libitum water intake in previously hypohydrated subjects did not affect urine flow or the decrease in [PVP]. The threshold [PVP] to initiate significant diuresis was about 2 pg x ml(-1), and significant diuresis can occur with no change in [PVP] maintained at about 1 pg x ml(-1) during immersion in euhydrated subjects. CONCLUSIONS: Thus, it appears that the Gauer-Henry reflex is not the major mechanism for immersion-induced diuresis. Clearly, other diuretic factors are also involved.

Adult↗
PubMed1975

[Treatment of resistant forms of cardiac insufficiency with a combination of diuretics].

The possibility of treating resistant forms of cardiac insufficiency by a combination of furosemide and brinaldix was studied. The efficacy of the diuretics was appraised with reference to diurnal diuresis, sodium-potassium- and chloruresis on the days of taking the diuretics. In making investigations the method of dispersion analysis (permutation trial test) was used. The final results show that the proposed combination (80 mg of furosemide and 40 mg of brinaldix) is effective and warranted in dealing with patients resistant to many diuretics including furosemide. The action of this combination continues for a long time in the presence of signs of cardiac incompetence and is not accompanied by the development of a marked hypokalemia.

Chlorine↗
PubMed1985

Effect of diuresis on urinary erythrocyte morphology in glomerulonephritis.

The differentiation between glomerular and non-glomerular haematuria by phase-contrast microscopy has proved to be a useful tool in the diagnosis of glomerulonephritis. In an attempt to evaluate the effect of marked diuresis on the altered red cell morphology in patients with biopsy proven glomerulonephritis, urinary sediments were examined following water or furosemide-induced diuresis. In both diuretic states urine flow increased, urine osmolality decreased and the percentage of glomerular erythrocytes was significantly reduced in the urinary sediment. These data demonstrate that the alteration in urinary red cells in glomerulonephritis is mainly caused by tubular forces. The diagnostic significance is reduced during increased diuresis and the evaluation of urinary red cell morphology should not be performed.

Adult↗
PubMed2004

An anti-aldosteronic diuretic component (drain dampness) in Polyporus sclerotium.

Polyporus Sclerotium botanically from the Polyporus umbellatus (PERS.) FRIES, was traditionally used for the purpose of promoting diuresis. The present study investigated the diuretic effect of ergosta-4,6,8(14),22-tetraen-3-one (ergone) which is a maker component according to the chemical assay for its quality standardization. It resulted in a reversion to ordinary value of the urinary ratio of Na/K in deoxycoricosterone acetate (DOCA)-treated and adrenalectomized rats, although it had no this effect on the Na or K contents as well as Na/K value both in normal rats and in adrenalectomized rats without DOCA. These data indicate that ergone possesses an anti-aldosteronic diuretic effect. Moreover, it was identified in the blood and bile of rats after its administration to the gastrointestinal tract. The above results demonstrate that it is an active component of Polyporus Sclerotium.

Animals↗
PubMed1991

Naloxone increases water and electrolyte excretion after water loading in patients with cirrhosis and ascites.

Endogenous opioids may be involved in the pathogenesis of ascites and edema in patients with liver cirrhosis. We administered the opioid antagonist naloxone (5 mg bolus followed by a 0.06 mg/min infusion) to eight male patients with alcoholic cirrhosis and ascites and to five healthy age- and sex-matched control subjects and determined the effects of naloxone on water and electrolyte excretion after a nonsustained water load (20 ml/kg). In comparison with saline vehicle infusion carried out in the same subjects, naloxone administration resulted in a 50% increase in urine output and creatinine clearance and twofold increases in sodium and potassium excretion in patients with cirrhosis. Fractional sodium and potassium excretion, minimal urinary osmolality, plasma vasopressin and aldosterone levels, arterial blood pressure, and heart rate were not affected by naloxone treatment. The diuretic effect of naloxone was not observed in control subjects. Plasma naloxone levels were about six times higher in patients with cirrhosis than in control subjects (probably because of impaired metabolism of the drug) but only a weak correlation was found between drug levels and the degree of diuresis observed. The diuretic effect of naloxone may be related to an increase in glomerular filtration rate, possibly in conjunction with altered tubular reabsorption.

Aged↗
PubMed1999

Urinary loss of thiamine is increased by low doses of furosemide in healthy volunteers.

Prolonged furosemide treatment is associated with urinary loss of thiamine and thiamine deficiency in some patients with congestive heart failure and low dietary thiamine intake. In the rat, diuretic-induced thiamine urinary loss is solely dependent on increased diuresis and is unrelated to the type of diuretic used. We studied the effects of single intravenous doses of furosemide (1, 3, and 10 mg) and of normal saline infusion (750 mL) on urinary thiamine excretion in 6 volunteers. Over a 6-hour period, furosemide induced dose-dependent increases in urine flow and sodium excretion rates (mean +/- SD), from 51 +/- 17 mL/h at baseline to 89 +/- 29 mL/h, 110 +/- 38 mL/h, and 183 +/- 58 mL/h (F = 10.4, P < .002) and from 5.1 +/- 2.3 mmol/h to 9.4 +/- 6.8 mmol/h, 12.1 +/- 2.6 mmol/h, and 20.9 +/- 10.6 mmol/h (F = 6.3, P < .005) for the three doses, respectively (104 +/- 35 mL/h and 13.0 +/- 6.2 mmol/h for the saline infusion). During this period the thiamine excretion rate doubled from baseline levels (mean of four 24-hour periods before the diuretic interventions) of 6.4 +/- 5.1 nmol/h to 11.6 +/- 8.2 nmol/h (F = 5.03, P < .01, for all four interventions, no difference being found between them), then returning over the following 18 hours to 6.1 +/- 3.9 nmol/h. The thiamine excretion rate was correlated with the urine flow rate (r = 0.54, P < .001), with no further effect of the type of intervention or sodium excretion rate. These findings complement our previous results in animals and indicate that sustained diuresis of >100 mL/h induces a nonspecific but significant increase in urinary loss of thiamine in human subjects. Thiamine supplements should be considered in patients undergoing sustained diuresis, when dietary deficiency may be present.

Adult↗
PubMed1984

Attenuation by d-ozolinone of l-ozolinone-induced diuresis in rats.

The effect of the non-diuretic dextrorotatory isomer of ozolinone on l- ozolinone -induced diuresis was studied in anesthetized rats. After intravenous application d- ozolinone attenuated l- ozolinone -induced increase in renal fluid, sodium, potassium and chloride excretion. Microperfusion experiments of the loop of Henle in vivo revealed that no interaction between the two stereoisomers occurred at this main site of tubular action of l- ozolinone . Since both isomers share the same organic acid transport pathway in the proximal tubule it is assumed that d- ozolinone attenuates the l- ozolinone -induced diuresis because it depresses proximal secretion of l- ozolinone and thereby partially prevents transfer of this diuretic to the tubular fluid.

Animals↗