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PubMed1994

Effects of chronic, urea-induced osmotic diuresis on kidney weight and function in rats.

To study the effects of chronic osmotic diuresis which were not associated with hyperglycaemia on the rat kidney, osmotic diuresis was induced by i.v. infusion of urea. A 5 mol/l urea solution was continuously infused at a rate of 100 ml.kg-1 x day-1 on the basis of body weight on day 0. Duration of infusion was 2, 6, 10 or 14 days. Control rats received continuously infused Ringer's solution. Urea-treated groups developed osmotic diuresis (urine flow = about 0.04 ml.min-1 x 100 g body weight-1) comparable to that in rats with experimental diabetes mellitus induced by i.v. streptozotocin (55 mg/kg), however urea-induced osmotic diuresis was not associated with blood glucose level increases. Compared with their controls, rats receiving urea for 2-14 days had markedly increased kidney weight. Rats receiving urea for 10 days showed greatest kidney weight increase, 0.565 +/- 0.044 g/100 g body weight (mean +/- SD), representing a 53% increase compared with the control (0.369 +/- 0.034 g/100 g body weight). Kidney weight was associated with increases in kidney protein content. In contrast, none of control kidney weight values differed significantly from day 0 values (= normal rats; 0.387 +/- 0.028 g/100 g body weight). Creatinine clearance values in urea-treated groups were also higher than those in controls. The maximum value, 0.65 +/- 0.17.ml-min-1 x 100 g body weight-1, was recorded in the 14-day group and was significantly higher than the corresponding control value (0.34 +/- 0.07 ml.min-1 x 100 g body weight-1) (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Pharmacokinetic studies of high-dose metoclopramide with and without forced diuresis.

The pharmacokinetics of high-dose metoclopramide (10 mg/kg body wt. in five infusions of 2 mg/kg body wt. each) was studied in 11 patients (5 females, 6 males) in two groups: group A with and group B (consisting of five patients) without forced diuresis. When the drug was infused, forced diuresis had no influence on the pharmacokinetics of metoclopramide (serum level after the 1st infusion was 851 +/- 361 ng/ml in group A versus 840 +/- 348 ng/ml in group B; after the 5th infusion it was 2,005 +/- 588 ng/ml in group A versus 2,463 +/- 1,350 ng/ml in group B). There were significant differences in the 24-h serum levels (582 +/- 308 ng/ml in group A versus 379 +/- 170 ng/ml in group B; P less than 0.05) and in the elimination half life (8.5 +/- 2.6 h in group A versus 6.1 +/- 1.1 h in group B; P less than 0.05). The results demonstrate that the dosage regimen originally suggested by Gralla for cytostatic drugs, with forced diuresis for high-dose metoclopramide therapy, may also be applied, with no dosage reduction, with to other cytostatic drugs which do not require forced diuresis.

Adult↗
PubMed1977

The effect of electrophoretic lignocaine blockade in the region of the carotid sinuses on spontaneous and water diuresis.

The effect of electrophoretic lignocaine blockade in the region of the carotid sinuses on changes in the intensity of spontaneous and water diuresis was investigated on anaesthetized dogs. After the blockade a reduction in spontaneous diuresis was observed and a marked and statistically significant restriction of water diuresis was noted as compared with the control experiments. The reduction in diuresis after the blockade was of a brief duration and did not appear to be related to changes in the intensity of the filtration through the kidneys, which was only slightly lower, but to changes in reabsorption. In all probability, the carotid blockade is connected with a dominance of hormonal effects by elimination of the effect of the nervi vagi, osmoreceptors of the carotid arteries and in particular the chemoreceptors of the carotid body.

Animals↗
PubMed1986

Significance of immediate diuresis in relation to transplant kidney survival rate.

Transplant kidney survival of recipients with immediate diuresis (n = 19) is compared with recipients who did not have a significant post-operative diuresis (n = 53). There is statistically no significant difference between patients without significant early diuresis (survival rate 71%) and patients with immediate diuresis (survival rate 68%, p greater than 0.1). The renal function was not different in the survivors of the two groups at 12 months post-transplant as measured by creatinine clearance (p greater than 0.35).

Creatinine↗
PubMed1980

Effect of osmotic diuresis on gentamicin-induced nephrotoxicity in rats.

The effect of isosorbide diuresis on gentamicin excretion and tissue accumulation as well as gentamicin-induced histopathologic changes in renal tissue were examine in rats. Gentamicin (30, 60, 120, 160 mg/kg) was administered s.c. for 10 consecutive days with or without isosorbide pretreatment. Osmotic diuresis with isosorbide did not significantly reduce the dose-dependent extent of gentamicin accumulation in renal tissues in comparison to nondiuresed rats. Although the urinary concentration of gentamicin was reduced in the diuresed animals, total gentamicin excretion remained unaffected. In addition, diuresis altered neither the renal excretion of the proximal tubular cell marker enzyme, N-acetyl-B-glucosaminidase, nor the severity of pathologic damage as determined by light microscopic examination of renal tissues. It appears that osmotically-induced diuresis alone is insufficient to prevent or significantly reduce gentamicin nephrotoxicity in rats. This is in contrast to other forms of diuretic therapy, such as furosemide, which have been shown to effectively reduce renal accumulation and resultant renal toxicity of aminoglycoside administration.

Acetylglucosaminidase↗
PubMed1986

Rapid diuresis in patients with ascites from chronic liver disease: the importance of peripheral edema.

Serial measurements of plasma volume and ascites volume were made during treatment with large doses of oral diuretics in 14 patients with stable chronic liver disease. Eight patients had pitting edema in addition to ascites. Reproducibility of ascites and plasma volume measurements was verified in 10 control subjects not receiving diuretics. Six patients without edema undergoing rapid diuresis lost a mean of 1.2 +/- 0.2 L of ascites and an equivalent amount of weight (1.3 +/- 0.4 kg) per day. All had a rise in blood urea nitrogen or creatinine, or both, and a fall in creatinine clearance. Eight patients with edema undergoing rapid diuresis lost more weight (1.8 +/- 0.5 kg/day, p = 0.06) but less ascites (0.7 +/- 0.35 L/day, p less than 0.05) than those without edema, and none developed renal insufficiency. After edema disappeared, ascites mobilization increased (1.4 +/- 0.7 L/day) and renal dysfunction occurred. Plasma volume fell an average of 24% +/- 9% in patients without edema but did not change in patients with edema (-0.4% +/- 3%). When edema disappeared, plasma volume fell significantly (28% +/- 8%, p less than 0.001). Electrolyte changes including hyponatremia, hyperkalemia, and hypochloremia were seen only in the group without edema. Patients with ascites and no edema are able to mobilize more than 1 L/day during rapid diuresis, but at the expense of plasma volume contraction and renal insufficiency. Patients with peripheral edema appear to be protected from these effects because of the preferential mobilization of edema and may safely undergo diuresis at a rapid rate (greater than 2 kg/day) until edema disappears.

Amiloride↗
PubMed1978

Nocturnal diuresis in panhypopituitarism.

Although impaired water diuresis in adrenocortical insufficiency is well-known, little attention has been paid to the diuretic pattern at night. In two cases of panhypopituitarism, the nocturnal diuretic pattern was found to be quite different from that in the morning, and marked diuresis did occur after water loading at night, without any significant change of serum cortisol which remained at a low level throughout the day. At the antidiuretic stage in the morning, urine osmolality continued to rise gradually, in spite of the water loading, to the level of 666 mOsm/liter. At the water restriction test, the urine was concentrated only to the same level of 600-700mOsm/liter. At the ascending stage of urine osmolality, exogenously injected pitressin showed little antidiuretic effect, although the kidney was able concentrate urine to the higher level later. In the morning, 3 liters of 5% glucose infusion failed to produce a marked diuresis in spite of extreme plasma dilution and expansion. Furosemide immediately induced diuresis even in the morning and the kidney recovered its ability to respond to pitressin. Glucocorticoid also improved the diuretic pattern in the morning, but a latent period of about 2 hr was always observed before the appearance of the effect. What happened during this latent period was unclear, but it was interesting to note that a mechanism similar to that which induces diuretic response seemed to occur without glucocorticoid at night.

Betamethasone↗
PubMed1988

Diuresis mediated by the superior laryngeal nerve in rats.

Diuresis mediated by the superior laryngeal nerve (SLN) was investigated using pentobarbital-anesthetized rats. A marked increase in urine flow was induced by application of water to the larynx. The diuretic effect of water was conspicuous during the first 30 min after the application and lasted for more than 1 hr. In contrast, a 160 mM solution of NaCl produced only slight diuresis. After bilateral sectioning of the SLNs, water-induced diuresis was considerably reduced. The results suggest that water fibers contained in the SLN may make a major contribution to the diuresis.

Animals↗
PubMed1992

Diuresis increases ascitic fluid opsonic activity in patients who survive spontaneous bacterial peritonitis.

Patients with low protein ascites and deficient ascitic fluid opsonic activity have been shown to be unusually predisposed to development of spontaneous bacterial peritonitis. Survivors of spontaneous peritonitis frequently develop recurrent infection. Diuresis has been shown to increase the ascitic fluid opsonic activity of patients who have never had spontaneous bacterial peritonitis. Patients with adequate opsonic activity are protected from ascitic fluid infection. Theoretically, the subset of patients who develop spontaneous peritonitis may have such severe liver disease that (i) their ascites is refractory to diuretic therapy or (ii) their ascitic fluid opsonic activity does not increase in response to diuresis. In this study, opsonic activity and concentrations of total protein and complement components were measured in the ascitic fluid of 11 patients who were hospitalized with spontaneous bacterial peritonitis and who responded to oral diuretics. The mean values of all of these parameters were found to increase significantly comparing the end-of-diuresis samples to the specimens that were diagnostic of ascitic fluid infection. Patients who survive spontaneous bacterial peritonitis are able to increase their ascitic fluid total protein and opsonic activity in response to diuresis. This increase in endogenous antimicrobial activity may help prevent recurrence of ascitic fluid infection.

Amiloride↗
PubMedDate not supplied

Norepinephrine-induced diuresis in chronically ethanol-treated rats.

Previous research from this laboratory indicated that noradrenergic mechanisms mediate ethanol diuresis. Experiments described here examined changes in sensitivity of these noradrenergic mechanisms in animals chronically treated with ethanol. Norepinephrine hydrochloride (0-12 micrograms intraventricularly) produced dose-dependent diuresis in control (dextrin maltose)- and ethanol (8-11 g/kg/day)-treated rats on the first day of treatment. Tolerance to ethanol diuresis was present after 10 days of ethanol treatment. Lack of responsiveness to norepinephrine-induced diuresis was evident only on the 20th day of treatment in both ethanol and dextrin-maltose groups of rats. These results suggest that norepinephrine does not play a primary role in the development of tolerance to the diuretic action of ethanol.

Animals↗
PubMed1983

Diuresis and pulmonary function in premature infants with respiratory distress syndrome.

A prospective study of 99 premature infants with severe respiratory distress syndrome who were randomly assigned to receive diuretic treatment with either furosemide or chlorothiazide was analyzed to examine the relationship of diuretic administration and diuresis to survival and to the duration and degree of mechanical ventilatory support. Subjects were given a diuretic, usually beginning on the second or third day of life, if they had not initiated the expected spontaneous diuresis and did not show pulmonary improvement. Infants given furosemide experienced a postnatal weight loss nearly identical to that in infants who were deemed not to need a diuretic; infants given chlorothiazide lost weight more slowly and had significantly greater body weight on postnatal days 4 and 5. Four factors were independently correlated with improved survival: furosemide usage, high birth weight, low initial mean airway pressure, and the absence of intraventricular hemorrhage. Ventilator mean airway pressure on the seventh day of life and duration of mechanical ventilation were both related to diuresis. These data provide additional evidence for the importance of water homeostasis in determining the course of respiratory distress syndrome in premature infants and indicate that furosemide administration is beneficial when spontaneous diuresis does not occur. Furosemide may be particularly effective if combined with early closure of the ductus arteriosus.

Chlorothiazide↗
PubMed1989

Surfactant therapy and spontaneous diuresis.

The effect of artificial surfactant therapy on renal function and the onset of spontaneous diuresis was prospectively evaluated in 19 infants with hyaline membrane disease in a double-blind, controlled study. Twelve infants were in the surfactant group; seven infants received placebo (0.9% saline solution). There was no difference in the time of onset of spontaneous diuresis (as defined by output greater than or equal to 80% of intake). The glomerular filtration rate, determined by endogenous creatinine clearance, was also similar in the surfactant- and placebo-treated infants during the first 3 days of life. The fractional excretion of sodium was significantly higher in the placebo group at 24 hours and 36 hours. Infants in the placebo group had a higher negative sodium balance than those in the surfactant group. Ventilatory status improved significantly soon after surfactant treatment, as evidenced by improvement in the alveolar/arterial oxygen pressure ratio and by a lower mean airway pressure. These data suggest that ventilatory status can be improved without diuresis; the factors that regulate diuresis are multiple and not fully understood.

Blood Gas Analysis↗
PubMed1994

Extensive urodynamic investigation: interaction among diuresis, detrusor instability, urethral relaxation, incontinence and complaints in women with a history of urge incontinence.

In 72 women with a clinical history of frequency and/or urge incontinence and in whom during filling cystometry nearly no abnormalities were detected, cystometry was repeated not by transurethral filling but under high diuretic conditions (diuresis cystometry). The prevalence and strength of detrusor instability, and the prevalence of incontinence were significantly greater during diuresis cystometry compared to filling cystometry. The experiences of these patients during episodes of instability were similar to those in their own daily environment. Most women with motor urge incontinence on filling or diuresis cystometry are losing urine at detrusor pressures lower than would be expected from urethral closure pressure measurements at rest. Therefore, urethral relaxation may have an important role in the etiology of incontinence. Apparent low amplitude detrusor instability may cause severe incontinence when combined with urethral relaxation. Extensive urodynamic investigations (including diuresis cystometry) will improve the clinical applicability of urodynamics.

Adult↗
PubMed1994

Comparison of urinary bladder function in rats with hereditary diabetes insipidus, streptozotocin-induced diabetes mellitus, and nondiabetic osmotic diuresis.

In vivo and in vitro bladder function were studied in three different models of increased diuresis: 1) Brattleboro rats with hereditary diabetes insipidus (di/di), 2) Sprague-Dawley rats with streptozotocin-induced diabetes mellitus (STZ), and 3) Sprague-Dawley rats with increased diuresis due to 5% sucrose added to the drinking water. When compared with controls, all three models showed bladder mass, increased water consumption and urine output, higher mean and maximal increased micturition volumes, and greater bladder capacity and compliance by in vitro cystometry. The changes were more extensive in di/di rats than in the STZ and sucrose-drinking rats. The concentration of bladder collagen decreased in all three rat models when compared with controls. However, the collagen concentration of STZ bladders was significantly lower than the collagen concentration of di/di and sucrose bladders, suggesting that the decrease in bladder collagen concentration associated with experimental diabetes mellitus is only partly related to the increased diuresis. Contractile function was studied using a whole bladder model. Responses of whole bladders from control and diabetic rats to electrical field stimulation, carbachol and KCl were identical. Volume-pressure relations of the isolated whole bladder showed that the magnitude of the contractile response to KCl is constant at intravesical volumes ranging from about 10 to 95% of cytometrical bladder capacity. Bladders from Brattleboro di/di rats and STZ rats showed a rightward shift of volume-passive pressure curves when compared with appropriate controls. Bladders from sucrose-drinking rats had volume-passive pressure curves similar to the bladders from controls. This study suggests that while contractile function remains intact with increased diuresis, the passive function changes, with the bladder becoming more distensible.

Animals↗
PubMed1975

Post-obstructive diuresis: a varied syndrome.

A prospective study was undertaken to define the clinical features, natural history and etiology of post-obstructive diuresis. Studied in detail were 8 patients with a massive diuresis after relief of urinary tract obstruction. We found that urea mediated osmotic diuresis, natriuresis owing to elimination of retained sodium from the obstructed phase, tubular defects in sodium reabsorption, renal unresponsiveness to antidiuretic hormone and iatrogenic factors may play varying roles in each individual diuresis. Overzealous fluid replacement should be avoided.

Adult↗
PubMed1982

Role of renal prostaglandins during antidiuresis and water diuresis in man.

The relationship of renal prostaglandins to antidiuretic hormone action and water diuresis was examined in 13 normal subjects and 2 subjects with diabetes insipidus. Following overnight water deprivation, a oral water load caused a prompt and sustained rise in the rate of urinary PGE2 excretion from 7.7 +/- 1.2 to 81.6 +/- 26.4 ng/hr (P less than 0.0001) in 7 normal subjects. Because the simultaneous increase in urinary excretion of urea was only 17% of the rise in urinary PGE2, passive wash-out of renal PGE2 probably accounts for only a small fraction of the increment in PGE2 excretion. Administration of the antidiuretic hormone analogue DDAVP to 6 normal subjects during sustained water diuresis resulted in a decrease in PGE2 excretion and urine flow rate comparable to that of dehydrated subjects. Thus, PGE2 excretion varied directly with urine flow rate over a wide range of states of hydration in all 13 normal subjects. One patient with central diabetes insipidus and one with nephrogenic diabetes insipidus demonstrated a similar positive correlation of PGE2 excretion rate and urinary flow rate in states of hydration, dehydration, and after administration of DDAVP. In the patient with nephrogenic diabetes insipidus, this relationship of PGE2 excretion rate to urine flow rate was unaffedted by DDAVP over a broad range of urine flow rates. Inhibition of prostaglandin synthesis with indomethacin in 6 normal subjects resulted in a significant decline in free water clearance (7.7 +/- 1.0 to 4.7 +/- 0.9 ml/min. P less than 0.001) and an increase in the minimal UOsm (61 +/- 4 to 93 +/- 19 mOsm/kg. P less than 0.01) achieved during water diuresis without a change in creatinine or osmolar clearances. Furthermore, the tightly linked relationship of PGE2 excretion rate to urine flow rate was reduced in 5 of 6 subjects during indomethacin treatment. We conclude that urinary PGE2 excretion varies directly with urine flow rate and is not directly dependent on ADH activity or state of hydration in man. The rise in PGE2 excretion during water diuresis may enhance the excretion of free water since indomethacin treatment blunted free water clearance while suppressing the rise in PGE2 excretion.

Adult↗
PubMed1994

Pressure-diuresis-natriuresis response in hyperthyroid and hypothyroid rats.

1. Renal responses to changes in renal perfusion pressure were studied in anaesthetized hyperthyroid (thyroxine, 300 micrograms day-1 kg-1) and hypothyroid (methimazole, 0.03% via drinking water) rats to determine whether an abnormality in the pressure-diuresis-natriuresis phenomenon is involved in the resetting of kidney function in these disorders. 2. There were no significant differences between control and hypothyroid rats with respect to the relationships between renal perfusion pressure and absolute or fractional water and sodium excretion. However, in hyperthyroid rats the pressure-diuresis-natriuresis mechanism was impaired. 3. Renal blood flow and glomerular filtration rate were well autoregulated and there were no differences between control and hypothyroid rats at every level of renal perfusion pressure. A significantly lower glomerular filtration rate was observed in hyperthyroid rats when data were expressed per gram kidney weight, but glomerular filtration rate was similar to that of control rats when normalized by body weight. 4. The shift in the pressure-diuresis-natriuresis response of hyperthyroid rats is mainly due to an increase in tubular reabsorption. Blunting of the renal pressure-diuresis-natriuresis mechanism in hyperthyroid rats may represent the functional resetting of the kidney necessary for sustained hypertension. However, a normal pressure-natriuresis response was observed in hypothyroid rats, in which blood pressure was markedly reduced.

Animals↗
PubMed1999

The role of nitric oxide in saline-induced natriuresis and diuresis in rats.

This study was designed to determine to what extent nitric oxide (NO) mediates the natriuretic and diuretic responses to acute isotonic saline (0.9 gram % NaCl) volume expansion (SVE, 0.5 ml min-1 kg-1). Studies were performed on 49 pentobarbital anesthetized (65 mg/kg) female Sprague-Dawley rats with or without a NO synthase inhibitor, Nomega-nitro-L-arginine (LNA). Group 1 received saline at 27 microliter/min for 1 hr (baseline) and then SVE for 1 hr; Groups 2-4 received LNA at 10, 150, and 200 microgram kg-1 min-1, respectively, for 1 hr followed by LNA + SVE. To determine to what extent inhibition of NOS would reverse an ongoing SVE-induced natriuresis and diuresis, Group 5 was saline-volume-expanded for hours 1 and 2 whereas Group 6 was administered SVE during the first hour and then SVE + 150 microgram kg -1 min-1 LNA during the second hour. SVE caused a significant (P < 0.05) increase in the glomerular filtration rate (GFR) of Group 1 and the LNA-treated rats (Groups 2-4). This SVE-induced increase in the GFR occurred despite the fact that baseline GFR was significantly lower in the two groups of rats that were infused with the highest doses of LNA (Groups 3-4). SVE was also associated with similar increases in urine flow rate, sodium and potassium excretion, and total osmolar excretion in Groups 1-4. On the other hand, mean arterial pressure (MAP) was significantly higher in Group 2 during SVE + LNA and during the baseline as well as during the SVE periods in Groups 3-4; MAP was also significantly elevated in Group 6 during SVE + LNA. Thus, despite the fact that MAP was higher in LNA-treated rats, sodium and urine flow rates were the same as in Group 1 (i.e., there was no evidence of a pressure natriuresis or diuresis in these animals). Along these lines, there was a small but significant positive linear correlation coefficient (r = 0.41, P = 0.05) between sodium excretion values and corresponding MAP values in SVE control rats but not in Groups 3-4 during SVE (r = 0.28, P = 0.26). The current data demonstrate that 1) NO does not mediate SVE-induced hyperfiltration in the rat, 2) NO also does not mediate SVE-induced natriuresis or diuresis, and 3), consistent with other reports, NO appears to mediate pressure natriuresis and diuresis.

Animals↗