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PubMed1996

Incidence of diuresis following hysterectomy.

Despite literature documenting ureteral obstruction associated with certain gynecological conditions, the occurrence of diuresis among posthysterectomy patients has not been examined. This nonexperimental exploratory study investigated whether diuresis was greater following hysterectomy for conditions that could potentially cause obstruction of the urinary tract than for other conditions requiring hysterectomy. Roy's adaptation model was used to emphasize the importance of expedient detection and intervention of the resultant fluid volume deficit. A retrospective chart review of 140 posthysterectomy patients was conducted. Four strata were used to divide the sample records into one nonobstructive and three potentially obstructive conditions for surgery. A ratio of total intake divided by total output was formulated for each patient and compared between the groups. Statistically significant differences were shown by one-way analysis of variance between two of the obstructive groups and the nonobstructive group (F = 5.182; P < .05). Results of this research showed that certain obstructive conditions--uterine prolapse/endometrial cancer and leiomyomas greater than 15 week size--were linked with substantially higher postoperative urine outputs, which increase the risk of hypovolemia.

Adult↗
PubMed1976

Effect of diuresis and nephron dimensional heterogeneity on the distribution of nephron filtration rates.

Conflicting data in studies of the effect of natriuresis on intrarenal single nephron glomerular filtration rate (SNGFR) redistribution may arise from the interplay of hitherto largely overlooked factors. In the present work, the effect of diuresis induced by saline, glucose or mannitol, as well as the effect of anatomical nephron heterogeneity, were studied. A highly significant positive correlation was found between the logarithm of the urine flow per gram of kidney weight (log V) and the mean superficial (S) to mean juxtamedullary (JM) SNGFR ratio. The rise in S/JM SNGFR with diuresis was primarily a function of decreased JM SNGFR. Total proximal tubular length (TPL) was used as a measure of nephron size. The distribution of nephron sizes was evaluated as S/JM TPL. The effects of urine flow and anatomical heterogeneity on S/JM SNGFR were spearated by means of multiple regression analysis, which yielded the following equation: S/JM SNGFR = -0.049 + 0.179 log V + 0.818 S/JM TPL. Both slopes were highly significant (P less than 0.001). These findings indicate that S/JM SNGFR increases with urine flow, independently of sodium homeostasis, and that anatomical heterogeneity has a marked effect and must, therefore, be controlled. Conflicting data in the literature are harmonized with the present data when appropriate correction can be made for the dimensional factor. There is no evidence that SNGFR redistributions play a role in sodium homeostasis.

Animals↗
PubMed1996

Effect of water diuresis and water restriction on expression of HSPs-27, -60 and -70 in rat kidney.

Expression of HSP-27, HSP-60 and HSP-70 was estimated in the cortex, outer medulla and inner medulla (papilla) of rats undergoing water diuresis or water restriction for two days. The mRNAs for HSP-27 and HSP-60 in renal papilla were two- to threefold greater in rats during water restriction than in those excreting a dilute urine, but levels of mRNA for HSP-70 were not reduced by water diuresis and Western analysis for HSP-70 protein showed no difference between water-loaded and water-restricted animals.

Animals↗
PubMed1997

Pressure diuresis and natriuresis in DOCA-salt mice.

The increasing use of mice in renal and cardiovascular studies has necessitated adapting physiological methods used for rats to mice, which are far smaller in size. We have adapted measurements of continuous renal blood flow, pressure natriuresis and diuresis, and laser-Doppler cortical and medullary flow to 40 g mice with DOCA-salt hypertension. We demonstrated a rightward shift in the pressure-natriuresis-diuresis curve. We conclude that with current, commercially-available equipment, sophisticated renal physiology can be conducted in the mouse. These methods will be important to investigations of gene-targeted mice.

Animals↗
PubMed2001

Lysosphingolipid receptor-mediated diuresis and natriuresis in anaesthetized rats.

Lysosphingolipids such as sphingosine-1-phosphate (SPP) and sphingosylphosphorylcholine (SPPC) can act on specific G-protein-coupled receptors. Since SPP and SPPC cause renal vasoconstriction, we have investigated their effects on urine and electrolyte excretion in anaesthetized rats. Infusion of SPP (1 - 30 microg kg(-1) min(-1)) for up to 120 min dose-dependently but transiently (peak after 15 min, disappearance after 60 min) reduced renal blood flow without altering endogenous creatinine clearance. Nevertheless, infusion of SPP increased diuresis, natriuresis and calciuresis and, to a lesser extent, kaliuresis. These tubular lysosphingolipid effects developed more slowly (maximum after 60 - 90 min) and also abated more slowly upon lysosphingolipid washout than the renovascular effects. Infusion of SPPC, sphingosine and glucopsychosine (3 - 30 microg kg(-1) min(-1) each) caused little if any alterations in renal blood flow but also increased diuresis, natriuresis and calciuresis and, to a lesser extent, kaliuresis. Pretreatment with pertussis toxin (10 microg kg(-1) 3 days before the acute experiment) abolished the renovascular and tubular effects of 30 microg kg(-1) min(-1) SPP. These findings suggest that lysosphingolipids are a hitherto unrecognized class of endogenous modulators of renal function. SPP affects renovascular tone and tubular function via receptors coupled to G(i)-type G-proteins. SPPC, sphingosine and glucopsychosine mimic only the tubular effects of SPP, and hence may act on distinct sites.

Anesthesia↗
PubMed1975

Paradoxical diuresis after vasopressin administration to patients with neurohypophyseal diabetes insipidus treated with chlorpropamide, carbamazepine or clofibrate.

1. Chlorpropamide, carbamazepine and clofibrate have an antidiuretic action in patients with neurohypophyseal diabetes insipidus which is qualitatively similar to that of antidiuretic hormone (ADH). 2. An additive antidiuretic effect is produced by combination of chlorpropamide and carbamazepine with small dosages of ADH. 3. After an immediate and transient antidiuresis, a single intravenous bolus injection of lysine vasopressin given during treatment with chlorpropamide, chlorpropamide with a continuous intravenous infusion of lysine vasopressin, carbamazepine or clofibrate, resulted in increased water diuresis for 12-24 h or longer. 4. This paradoxical diuresis was not observed during treatment with chlorothiazide. 5. It is suggested that the antidiuretic action of chlorpropamide, carbamazepine and clofibrate is localized at the receptor site for ADH in the distal renal tubular cell.

Adolescent↗
PubMed1978

Effects of renal dopamine receptor and beta-adrenoreceptor blockade on rises in blood angiotensin after haemorrhage, renal ischaemia and frusemide diuresis in the dog.

1. In chloralose-anaesthetized dogs, central venous and arterial angiotensin (AII) levels were monitored by blood-bathed bioassay during venous haemorrhage of 20 ml/kg, acute renal ischaemia induced by suprarenal aortic stenosis and frusemide-induced diuresis. 2. Blockade of intrarenal dopamine receptors with ergometrine reduced markedly the increments in arterial AII associated with haemorrhage or suprarenal aortic stenosis, but did not consistently affect the corresponding increments in venous AII. 3. Ergometrine or renal denervation did not affect the increases of blood AII associated with frusemide diuresis. 4. Blockade of beta-adrenoreceptors with propranolol, by contrast, reduced blood AII increments associated with all three procedures. 5. It is suggested that renin release during moderate haemorrhage and acute suprarenal aortic stenosis is, in the dog, partly due to activation of intrarenal dopaminergic nerves. 6. The possibility is discussed that propranolol may depress renin release in the dog by an action other than that of blocking beta-adrenoreceptors.

Angiotensin II↗
PubMed1985

The causative agent in atrial receptor diuresis in the dog is a low molecular weight, lipophilic and weakly acidic substance.

Stimulation of atrial receptors by distension of a balloon in the left atrium of anaesthetized dogs results in a reflex diuresis mediated by a humoral agent of unknown identity. In previous investigations, a substance was recovered in a low molecular weight fraction from Bio-Gel P-2 (100-1800 daltons) and shown to be related to the reflex diuresis. In this investigation, the active Bio-Gel P-2 fraction was partitioned with ethyl acetate at pH 11.0, with subsequent partition of the aqueous phase with ethyl acetate at pH 7.4; the activity of the humoral agent was soluble in ethyl acetate at pH 7.4. These investigations suggest that the humoral agent is a low molecular weight, lipophilic and weakly acidic substance. The substance is not antidiuretic hormone (ADH) as vasopressin is insoluble in ethyl acetate at pH 7.4.

Acetates↗
PubMed1986

Implication of thromboxane in frusemide diuresis in rats.

Administration of the thromboxane A2 (TXA2) synthase inhibitor OKY 1581 to rats significantly increased the urine output elicited by the loop diuretic frusemide. The administration of the TXA2 receptor antagonist SQ 29548 significantly increased the diuretic effect of frusemide. Another TXA2 receptor antagonist L-640,035 increased significantly the diuretic effect of frusemide. Both the sodium excretion rate and urine osmolar excretion rate were significantly increased in rats treated with the TXA2 synthase inhibitor OKY 1581 and frusemide. The data suggest that TXA2 is released during frusemide-induced diuresis in rats, and the released TXA2 has an opposing antidiuretic effect. Key words: antidiuretic hormone, frusemide diuresis, thromboxane inhibitor and antagonists.

Animals↗
PubMed2002

Induction of fetal diuresis with intraamniotic furosemide increases the clearance of intraamniotic substances: An alternative therapy aimed at reducing intraamniotic meconium concentration.

BACKGROUND/PURPOSE: Contact with amniotic fluid (AF) causes intestinal damage in gastroschisis. Intraamniotic meconium has been shown to be responsible for intestinal damage, and occurrence of this damage has been shown to depend on the concentration of intraamniotic meconium. When intraamniotic meconium concentration is lowered below threshold level by exchanging AF with saline in gastroschisis, intestinal damage can be prevented. Theoretically, induction of fetal diuresis with intraamniotic furosemide may increase AF volume and fetal swallowing rate, thus, increase absorption of AF by intestines; therefore, the clearance of meconium from the AF may increase. An experimental study was planned to investigate the effects of intraamniotic diuretic injection on the clearance of intraamniotic substances. METHODS: Pregnant rabbits on the 23rd to 25th gestational day were divided into 2 groups as furosemide and control. Technetium tc99m labeled "tin colloid" was injected into the amniotic cavity, and AF sample was taken 10 minutes later. Furosemide was injected into the amniotic cavity afterwards. Two and 6 hours later, AF samples were obtained. Intestines were harvested at the end of the study. Control group received intraamniotic saline instead of furosemide. Radioactivities of the AF samples and intestines were determined by gamma counter. Clearance of the radioisotope from AF and intestinal accumulation were calculated. RESULTS: The clearance of the radioisotope from AF was increased significantly in the furosemide group (n = 10) compared with the control group (n = 8; P <.01). Gastrointestinal accumulation of the radioisotope in the furosemide group was 4-fold higher than that the control group (P <.01). CONCLUSIONS: Induction of fetal diuresis with intraamniotic furosemide accelerates the clearance of intraamniotic substances. This is probably caused by increased urinary output rate, which increases AF volume and consequently results in increased fetal swallowing of AF. In the diseases like gastroschisis and myelomeningocele, in which the contact with AF causes tissue damage, the elimination of meconium from AF in a somewhat natural manner like this method, should be studied further because it may be an alternative minimal invasive in utero treatment modality.

Amniotic Fluid↗
PubMed1996

[The diuresis urogram in patients with a bladder replacement].

PURPOSE: To differentiate between urodynamically relevant obstruction and functionally unimportant dilation of the upper urinary tract in patients with neobladder using a modified furosemide urogram. METHOD: An excretory urogram with furosemide loading was carried out in 19 patients with neobladder and sonographically and urographically confirmed dilation of the upper urinary tract. Once strong contrasting of the renal pelves and calyces has been achieved, 20 mg of furosemide were applied and late radiographs were obtained at 15 min and 30 min, respectively. An obstruction was defined as increasing dilation of the renal pelves and calices during forced diuresis and lack of washout effect of the contrast medium. RESULTS: In 32 cases, the renoureteral unit (RUU) was dilated on ultrasound. Of these, 25 RUU's showed good emptiness of contrast medium upon stimulation of diuresis, six RUU's returned a borderline findings, while one RUU was found to exhibit a decompensated anastomotic stenosis, which was dilated. Two further patients with borderline findings were later treated surgically due to their pain symptoms. No patient required further preoperative diagnostic procedures. CONCLUSIONS: The modified furosemide urogram represents a cost-effective diagnostic orientation strategy in patients with neobladder and dilated renal pelves and calyces and is both well-tolerated by patients and meets with broad acceptance from the urologic staff.

Adult↗
PubMed1997

Reinvestigation of water diuresis in the rat: role of anesthesia and acute surgery.

Renal effects of water loading on urine flow rate (V) and concentration (Uosm) were studied in Wistar rats subjected to minor or extensive surgery, under different kinds and level of anesthesia. In the explanted kidney of chronically prepared rats, under light chloralose anesthesia, 1 h.i.v. hypotonic fluid load increased V of the experimental (left) kidney 11 fold while Uosm decreased from 1181 +/- 142 to 210 +/- 80 mosm kg/H2O. In the acutely exposed kidney, under Inactin anesthesia, V increased 5 fold and Uosm decreased from 785 +/- 170 to 204 +/- 57 mosm/kg H2O. In similar experiments under Nembutal anesthesia V increased 4 fold but the urine did not become hypotonic. After acute surgery under Inactin anesthesia water diuresis can be induced but urine concentration before water loading is impaired. Urine hypotonicity after water loading is not achieved in acute experiments under Nembutal--an unsuitable approach to studies of water diuresis. Thus, a transition from antidiuresis to urine dilution can best be accomplished in the chronic explanted kidney model under light anesthesia and without invasive surgery.

Anesthesia↗
PubMed1988

On the mechanism of acute tolerance to furosemide diuresis.

The renal response to continuous furosemide infusion (8 mg/h) and subsequent ECV changes was studied in 8 healthy volunteers. Furosemide increased urine flow from a basal flow of 4.3 ml/min to a maximum of 15.4 ml/min. During dehydration (-1.8 kg) the diuresis decreased to 8.4 ml/min. The sodium, chloride and potassium excretion likewise decreased. This reduction in diuretic effect (acute tolerance) was accompanied by significantly increased plasma levels of norepinephrine (1.38 to 2.14 nmol/l), PRA (0.52 to 1.13 ng/ml/h) and aldosterone (0.29 to 0.45 nmol/l). After rehydration the urine flow increased to 23.1 ml/min. The changes in diuretic response from initial effect to the dehydrated state and after rehydration were mainly a consequence of changed renal sensitivity to furosemide (urinary excretion of 21 to 14 to 35 mumol Na+ per microgram furosemide excreted). It is proposed that activation of the sympathetic nervous system and/or the renin-angiotensin-aldosterone system may play a role in mediating the acute tolerance to furosemide diuresis. The relative importance of each remains to be clarified.

Adult↗
PubMed1976

Kidney function during hydropenia nad water diuresis in patients with idiopathic recurring nephrolithiasis.

The kidney function of 41 patients with idiopathic recurring kidney stones was investigated by inulin- and PAH-clearances and by measuring the excretion of electrolytes during hydropenia and water diuresis. All patients had normal inulin- and PAH-clearances and normal concentrating capacity as indicated by free water reabsorption (Tc H2O). Seven patients, all of whom had previously been found to have low excretion of magnesium in urine, were unable to dilute their urine. During water diuresis these patients also had lower osmolar clearance and lower excretion of sodium than the other patients. A defective dilution capacity may be of pathogenetic significance for stone formation; the causes of the defect, however, are not clear.

Adult↗
PubMed1987

Diuresis bacteriuria in physically dependent elderly women.

Among 34 women aged 74-96 years, residents of a Home for the Aged, with reduced mobility and repeatedly negative urine cultures, 16 (47%) responded to a rapid hydration and 20 mg frusemide administered intravenously with a transient bacterial excretion usually trailing the diuresis. Antibody-coated bacteria were detected in 11 of the 13 Gram-negative isolates tested. Women with urine turning positive had significantly lower glomerular filtration rates and more advanced renal tubular defects than the steadily nonbacteriuric subjects of the same age. Progress to renal insufficiency was somewhat faster and all-causes mortality at 1 year was higher in subjects with urine turning positive. Diuresis bacteriuria originating from the upper urinary tract along with frank bacteriuria may be detected in up to 70% of women in their mid-80s and represents a likely source of the most common infection in man's last period of life.

Activities of Daily Living↗
PubMed1996

Synergistic renal protection by combining alkaline-diuresis with lipid peroxidation inhibitors in rhabdomyolysis: possible interaction between oxidant and non-oxidant mechanisms.

BACKGROUND AND PURPOSE: Heme-proteins, besides causing renal tubular obstruction, may contribute to rhabdomyolysis-induced renal injury through a heme-iron-mediated lipid peroxidation process. In the present study, we compared the combined therapy of a lipid peroxidation inhibitor, 21-aminosteroid (21-AS) and fluid-alkaline-mannitol (FAM) diuresis with either of them alone to determine the efficacy of the combination therapy and to delineate the roles of lipid peroxidation and cast formation. METHODS AND RESULTS: Employing Raman spectroscopy, we confirmed in vitro the ability of 21-AS to inhibit iron-induced fatty acid peroxidation. 21-AS was then administered to rats developing renal failure from glycerol-induced rhabdomyolysis. Although 21-AS inhibited rhabdomyolysis-induced plasma and renal lipid peroxidation, renal protection was incomplete. Administration of FAM to inhibit cast formation afforded a better renal protection. However, when these therapies were combined to inhibit both lipid peroxidation and cast formation, there was a synergistic renal functional protection. This was accompanied by a maximum inhibition of renal and plasma lipid peroxidation, as well as, renal tubular necrosis and cast formation. Compared to combination therapy, FAM therapy alone, despite identical volume, was accompanied by a higher tubular necrosis and cast formation. CONCLUSIONS: That combining a lipid peroxidation inhibitor with fluid-alkaline diuresis in rhabdomyolysis further lowers renal lipid peroxidation, tubular necrosis and cast formation and synergistically limits renal dysfunction (i) supports a role for lipid peroxidation in the pathophysiology of rhabdomyolysis ARF, (ii) underscores the role of the intratubular heme retention, a cause for tubular obstruction as well as a source for prodigious amount of iron, likely involved in the lipid peroxidation, and (iii) raises the possibility of interactions between non-oxidant and oxidant mechanisms.

Acute Kidney Injury↗
PubMed1988

Compensatory pressor role of vasopressin following acute diuresis.

Recent interest has focused on the role of vasopressin (AVP) in blood pressure (BP) regulation. This study was performed to determine if vasopressin has a compensatory pressor role following acute diuresis in both normal rats and in rats with subtotal nephrectomy (SN) or in rats with SN-salt induced hypertension. An inhibitor (AVP-I), specific for the AVP vascular smooth muscle receptor, was administered intravenously to assess the AVP dependency of the BP. Furosemide administration significantly increased plasma AVP levels in all rats. Administration of AVP-I did not change BP in the normal rats with or without prior furosemide administration or in the SN rats without furosemide administration. In contrast, after furosemide administration, AVP-I significantly decreased mean BP in the SN rats. The administration of AVP-I to the SN-salt hypertensive rats, with or without furosemide administration, significantly decreased mean BP. In conclusion, AVP has a compensatory pressor role in SN rats after acute diuresis, with or without salt-induced hypertension, but not in the normal rat.

Animals↗
PubMed1990

Caffeine-induced diuresis and atrial natriuretic peptides.

After a single-blind, randomized, cross-over protocol using decaffeinated coffee in a control experiment, the effect of an oral 250-mg caffeine dose on plasma immunoreactive atrial natriuretic peptide (ANF) was assessed in eight healthy students who had been on a methylxanthine-free diet for 1 week. One to 2 h after caffeine ingestion, both systolic blood pressure (SBP) and diastolic BP (DBP) increased by 12 mm Hg while heart rate (HR) also tended to increase. An increase in diuresis and in urinary sodium, potassium, and osmol excretion was observed within 1 h. Decaffeinated coffee induced no change in any of these parameters. Plasma epinephrine (EPI) increased gradually from 16.6 +/- 3.2 pg/ml (mean +/- SEM) to 45.1 +/- 7.9 pg/ml within 2 h after caffeine ingestion, but did not change after decaffeinated coffee (p less than 0.001). Plasma norepinephrine (NE), renin activity (PRA), aldosterone, and vasopressin remained unchanged. Plasma ANF was measured by radioimmunoassay (RIA) using an extremely sensitive antiserum (Kd = 10(-12) M) after rapid and virtually complete (90-103%) extraction from plasma. In 0.2 ml plasma, the theoretical detection limit is 1.1 fmol/ml. Normal plasma ANF concentrations in supine subjects were 17.9 +/- 8.1 fmol/ml (mean +/- SD) and 11.0 +/- 3.3 fmol/ml in subjects in the upright position. Plasma ANF levels were not affected by coffee drinking. In conclusion, by using a new and sensitive assay for plasma ANF, we did not find that caffeine-induced diuresis is mediated by ANF.

Adult↗