Changes In Urine Output Research Articles

COMPARISON OF THE EFFICACY OF CONTINUOUS FUROSEMIDE AND LOW-DOSE DOPAMINE INFUSION IN PREECLAMPSIA/ECLAMPSIA-RELATED OLIGURIA IN THE IMMEDIATE POSTPARTUM PERIOD

Aim: To compare the efficacy of furosemide infusion with that of low-dose dopamine infusion in improving urine output and subsequent renal function in preeclamptic/eclamptic patients with oliguria in the immediate postpartum period. Design: Prospective randomised single blind clinical trial. Setting: Obstetric High Care Unit of King Edward VIII Hospital, a large referral tertiary hospital. Method: Eighty postpartum patients with severe preeclampsia/eclampsia with oliguria were enrolled. Hypovolaemia was corrected under central venous pressure (CVP) monitoring and urine output monitored for 4 hr. Patients who remained oliguric were randomly assigned to a continuous infusion of low-dose dopamine (3 μg/kg/min), or furosemide 5 mg/hr infusion, for 12 hr. In patients with no response after 12 hr, the drugs were switched and continued for a further 12 hr. A subgroup of patients who responded 4 hr after correction of hypovolaemia was observed for 12 hr. The primary outcome measured involved the comparison in urine output between the different drug regimes and the number of patients requiring haemodialysis. Secondary outcome measures involved assessment of serum urea and creatinine values in the two treatment groups. Results: Of the 80 patients enrolled, 20 improved their urine outputs within the 4-hr observation period. Sixty patients were randomised to furosemide or low-dose dopamine infusion. There was no statistical significant difference in the mean hourly urine output, rate of change in urine output over time and the mean urea or creatinine levels between the treatment groups. Ten percent of patients that failed on furosemide primarily, and 8.5% of patients that failed on initial low-dose dopamine, received haemodialysis. The difference in demographic and clinic data between these groups was not statistically significant. Conclusion: Administration of continuous infusion of furosemide showed comparable efficacy to low-dose dopamine infusion in ameliorating oliguria in severe preeclampsia/eclampsia post delivery; there was no difference in the percentage of patients that required haemodialysis in either group.

Downregulation of AQP1, -2, and -3 after ureteral obstruction is associated with a long-term urine-concentrating defect.

Previously, we demonstrated that 24 h of bilateral ureteral obstruction (BUO) and short-term release of BUO was associated with a decrease in the expression of aquaporin-2 (AQP2), polyuria, and a reduced urinary concentrating capacity (10). The purposes of the present study were to examine whether BUO and the long-term release of BUO (BUO-R) for 3, 14, and 30 days were associated with changes in the expression of renal AQP1, AQP2, and AQP3 and whether such changes were associated with parallel changes in urinary output and urinary concentrating capacity. Rats (n = 4-7 in each group) were kept in metabolic cages for measurements of urinary output. Kidneys were removed to determine the expression levels of AQP1, AQP2, and AQP3 by semiquantitative immunoblotting. AQP2 was downregulated after 24 h of BUO (42 +/- 3%). Downregulation of AQP2 persisted 3 (43 +/- 14%; P < 0.01) and 15 days after BUO-R (48 +/- 11%; P < 0.01) but was normalized 30 days after BUO-R. AQP3 showed a similar pattern. Moreover, AQP1 was downregulated in response to BUO (65 +/- 7%) and remained downregulated 3 days after BUO-R (41 +/- 5%), 14 days after BUO-R (57 +/- 8%), and 30 days after BUO-R (59 +/- 5%). BUO-R resulted in a significant polyuria that gradually decreased, although it remained significant at day 30. Urinary concentrating capacity remained significantly impaired when determined 3, 14, and 30 days after BUO-R in response to a 24-h period of thirst (1,712 +/- 270 vs. 2,880 +/- 91 mosmol/kgH2O at day 30, P < 0.05). In conclusion, the expression of AQP1, AQP2, and AQP3 were long-term downregulated after BUO-R, suggesting that dysregulation of aquaporins located at the proximal tubule, thin descending limb of the loop of Henle, and the collecting duct may contribute to the long-term polyuria and impairment of urinary concentrating capacity associated with obstructive nephropathy.

Inositol Phosphoglycans and Signal Transduction Systems in Pregnancy in Preeclampsia and Diabetes: Evidence for a Significant Regulatory Role in Preeclampsia at Placental and Systemic Levels

Measurements have been made of the urinary content of inositol phosphoglycans IPG P-type and IPG A-type, putative insulin second messengers, in preeclampsia, in type I insulin-treated diabetic pregnant women and their matched control subjects, and nonpregnant women of child-bearing age. The content of IPG P-type and IPG A-type was also measured in the placenta from preeclamptic patients and from normal pregnancies. Pregnancy was associated with an increase, approximately twofold, in urinary output of IPG-P-type relative to nonpregnant controls (P < 0.01). The 24-h output of IPG P-type in urine in preeclamptic women was significantly higher (2- to 3-fold) than in pregnant control subjects matched for age, parity, and stage of gestation (P < 0.02). In contrast, insulin-dependent diabetic pregnant women did not show any significant change in urinary output of IPG P-type or IPG A-type relative to pregnant control subjects. Evidence for a possible relationship and correlation between the urinary excretion of IPG P-type and markers of preeclampsia, including proteinuria (r = 0.720, P < 0.01), plasma aspartate transaminase (r = 0.658, P < 0.05), and platelet counts (r = 0.613, P < 0.05) is presented. A high yield of IPG P-type was extracted from human placenta, in preeclampsia some 3-fold higher (P = 0.03) than the normal value, whereas no IPG A-type (with lipogenic-stimulating activity) was found. Low concentrations of placental IPG A-type were detected relative to IPG P-type using assay systems dependent upon the effect of this mediator on cAMP-dependent protein kinase or on a proliferation assay using thymidine incorporation into DNA of EGFR T17 fibroblasts. It is postulated that the high urinary excretion IPG P-type in preeclampsia reflects high placental levels and relates to the accumulation of glycogen in the placenta. The paracrine effects of placental IPG P-type (stimulation off other endocrine glands and/or endothelial cells) could contribute to the pathogenesis of the maternal syndrome. A possible theoretical link between elevated placental IPG P-type and apoptosis is proposed.

Power Doppler ultrasonography compared with scintigraphy in the diagnosis of renal allograft dysfunction

POWER Doppler imaging is based on the integrated power of the Doppler signal as opposed to mean frequency shift, the feature used in color Doppler imaging. The power Doppler modality has several advantages over color Doppler, including angle independence, the absence of aliasing, and extended dynamic range. As a result of these benefits, power Doppler ultrasonography is sensitive to low-velocity blood flow in small vessels. Marked blood flow alterations in renal transplants can occur before a recipient shows any change in urine output. Intimal thickening in arteries leads to progressive ischemia of the cortex in acute and chronic renal graft rejection. Decreased outer cortical flow on the power image and decreases in mean value on the power histogram have been documented in patients with chronic transplant rejection. Impaired perfusion is manifested as decreased amplitude of the power Doppler signal. Calculation of a perfusion index using Tc-99m-labeled compounds can be used as an indicator of renal blood flow. Our aim was to investigate renal transplant dysfunction using power Doppler sonography and scintigraphy, and to compare these modalities by relating the respective findings to core biopsy results.

Aminophylline in the treatment of fluid overload

Aminophylline has not been studied as an adjunct diuretic in critically ill children. Our purpose was to evaluate its use in the treatment of fluid overload in these patients. Open, controlled clinical trial. Pediatric intensive care unit. Study subjects ranged from 2-46 months of age, were fluid overloaded, and were receiving a continuous infusion of furosemide (> or =6 mg/kg/day). Patients with hemodynamic instability or liver dysfunction were excluded. A single dose of aminophylline (6 mg/kg) was given after establishing baseline values. There were no additional diuretics or changes in vasoactive agents during the study. Urine output, creatinine clearance, and sodium and potassium excretion were measured before and after administration of the aminophylline bolus. Heart rate and mean arterial pressure (mm Hg) were recorded hourly. Urine output increased by >80% (p < .01) during the first 2 hrs after administration of the aminophylline bolus and then returned to baseline by 4 to 6 hrs. The change in urine output is consistent with the pharmacokinetics of aminophylline. Heart rate and mean arterial pressure exhibited a change of <10% from baseline. These results suggest that aminophylline is an effective adjunct to furosemide in increasing diuresis in critically ill children with fluid overload. The increased diuresis can be accomplished without increased risk if drug levels are adequately monitored.

Changes in urinary output during laparoscopic adrenalectomy.

To better understand the physiological effects of pneumoperitoneum, by examining changes in urinary output during gaseous and gasless laparoscopic adrenalectomy. Laparoscopic adrenalectomy was performed with gas in six patients and without in three. Urinary output was measured during insufflation and after desufflation. In all patients who received gas, the urinary output was significantly decreased during insufflation and significantly increased after desufflation. However, there were no changes in urinary output in patients who did not receive gas. For the safety of laparoscopic surgery it is important to recognise that oliguria occurs during pneumoperitoneum, although the changes in urinary output caused no complications in renal function.

Metabolic Consequences in very Low Birth Weight Infants Transfused with Older As-1-Preserved Erythrocytes

Our study evaluated the biochemical and physiologic changes in extremely premature infants receiving AS-1-preserved packed red blood cells (PRBC) stored 5 to 21 days, including increase in hemoglobin, maintenance of euglycemia, and normal serum potassium levels, acid-base balance, and urine output. Twelve infants (birth weight 775 ± 127g) with gestational age of 25 ± 1 weeks received small volume replacement transfusions with 17 mL/kg PRBC preserved in an AS-1 dedicated unit. Infants were monitored throughout the transfusions and blood samples were obtained pre- and postransfusion for comparison by Student's t-test. The infants remained clinically stable throughout the transfusions and had an increase in hemoglobin of 2.5 g/dL. There was no change in urine output. Serum ammonia lactate dehydrogenase (LDH), and glucose levels were altered as predicted. There were also small, but clinically insignificant, changes in serum potassium, bicarbonate, total bilirubin, and creatinine. Euglycemia was maintained in ...

A Case of Nonoliguric Renal Failure After General Anesthesia with Sevoflurane and Desflurane

A Case of Nonoliguric Renal Failure After General Anesthesia with Sevoflurane and Desflurane

Urinary adenosine excretion in patients receiving amphotericin B

Background. Intravenous amphotericin B (AMB) administration in animals causes renal vasoconstriction, ischemia, and oliguria that may result in irreversible renal injury; the mechanism of AMB nephrotoxicity may be similar in human beings. Adenosine is excreted in urine by the ischemic kidney. We hypothesized that adenosine excretion and oliguria would be a marker for patients who later would manifest AMB-associated renal insufficiency and that pre-AMB saline administration (which ameliorates AMB nephrotoxidty) would negate the change in adenosine excretion and urine output. Methods. Twenty hospitalized patients being treated at the direction of their attending physician and who were receiving AMB (15 to 75 mg intravenously) had urine collected for 1 hour before and for 2 hours during AMB infusion. Eleven patients received normal saline solution (500 ml intravenously) before the AMB infusion; the other nine formed the comparator group. An aliquot of each urine collection was precipitated with perchloric acid to remove protein and cellular elements and centrifuged, and the supernatant was assayed for adenosine by using high-pressure liquid chromatography. Results. Infusion of AMB was associated with a decrease in mean urine output both in patients who received saline solution (245 before versus 149 ml/hr during AMB infusion, p = 0.04) and in patients in comparator group (139 versus 89 ml/hr, p = 0.027). The mean urinary adenosine excretion was unchanged in the saline-loaded group (0.1354 before versus 0.1255 mmol/hr during drug infusion, p = 0.25) and was decreased in the comparator group (0.2276 versus 0.1127 mmol/hr, p = 0.01). Development of renal insufficiency did not correlate with the change in urine output or adenosine excretion. Conclusions. AMB infusion in human beings results in decreased urine output and decreased adenosine excretion. The latter effect is prevented by a pre-AMB saline load. The changes in urine output and adenosine excretion are not predictive of the development of renal insufficiency.

The role of carotid chemoreceptors in the effects of hypoxia on renal blood flow in the late gestation sheep fetus.

Previous studies of the effect of hypoxia on fetal renal haemodynamics have demonstrated a fall, a rise or no change in renal blood flow (RBF). The underlying mechanisms are not understood but involve a balance between neural vasoconstrictor and opposing vasodilator mechanisms. Since carotid chemoreflex mechanisms contribute to vasoconstriction in other fetal vascular beds and in the adult renal vasculature, we examined their effects on RBF during 1 h of acute hypoxia in late gestation fetal sheep (n = 12). Renal blood flow was measured continuously and urine collected at 15 min intervals. Seven fetuses underwent bilateral section of the carotid sinus nerves (CSD fetuses). During hypoxia CSD fetuses showed a transient initial rise in RBF (P < 0.05) and then a subsequent fall (P < 0.05) to levels comparable with that recorded in intact fetuses. There was no change in urine output in either intact or CSD fetuses during hypoxia. Thus the initial fall in RBF during hypoxia is a carotid chemoreflex but other mechanisms, e.g. vasoconstrictor hormones, contribute to the sustained response.

Changes in urinary output and electrolytes during gaseous and gasless laparoscopy.

Urological laparoscopy has gained increasing acceptance recently. Alterations in renal water and electrolyte homeostasis by carbon dioxide peritoneal insufflation, retroperitoneal insufflation and abdominal wall lifting were measured in 30 well-hydrated pigs over a 2-h period. Oliguria was observed after gaseous insufflation but not alter lifting the abdominal wall. Return to normal urinary output was observed at 30 min after release of pneumoretroperitoneum, and 60 min after pneumoperitoneum. Creatinine clearance declined, while the clearance rates of potassium, sodium and urea remained unchanged during peritoneal and retroperitoneal insufflation. An elevated serum aldosterone concentration was found which may mediate the increased urinary excretion of potassium and decreased urinary excretion of sodium found during peritoneal insufflation. Renal function remained stable, despite an elevation of serum creatine kinase being elicited after lifting the abdominal wall. In conclusion, significant changes in water and electrolyte homeostasis occurred gaseous, not gasless, laparoscopy in pigs.

Oliguria during laparoscopic surgery: evidence for direct renal parenchymal compression as an etiologic factor.

Abdominal insufflation during laparoscopy has been associated with transient oliguria, which abates after desufflation. Direct renal compression evoking a Page kidney effect was proposed as a mechanism. In an effort to confirm this theory, the left kidney was subjected to 15 mm Hg compression in six anesthetized mongrel dogs. For this, a pressure cuff was placed around the kidney excluding the renal hilar structures. The contralateral kidney was left untouched to serve as a control. After a steady-state period, the pressure cuff was inflated to 15 mm Hg for 2 hours. Cuff desufflation was followed by a 1-hour recovery period. Urine output, glomerular filtration rate (GFR), and effective renal blood flow (ERBF) were measured for both kidneys during each clearance period. For the treated kidneys, the mean urine output decreased 63% (P < 0.05) during compression and increased 109% (P < 0.05) after cuff desufflation. The GFR decreased 21% (P < 0.01) during compression and increased 25% (P < 0.05) during recovery. The ERBF decreased 26% (P < 0.05) during compression, and during the 1-hour recovery period, ERBF did not recover to baseline values. For the control kidneys, there were no significant changes in urine output or GFR during the experimental and recovery periods. These data support the view that direct renal parenchymal compression is an important factor in the development of insufflation-induced oliguria. The clinical implications of insufflation-induced oliguria during laparoscopy deserve further investigation.

Identification of α1-adrenoceptor subtypes involved in the antinatriuretic response to intrarenal infusion of phenylephrine

It is reported that α 1-adrenoceptors located in the renal vasculature and renal tubules play a major role in mediating antinatriuretic response to renal nerve stimulation as well as to the infusion of α 1-adrenoceptor agonist. In the present study intrarenal infusion of α 1-adrenoceptor agonist phenylephrine (0.25 μg/kg/min) to Inactin-anesthetized Sprague-Dawley rats produced approximately 50% reduction in urine output, Na + excretion and glomerular filtration rate without causing significant alterations in mean blood pressure, heart rate and fractional Na + excretion. These changes were completely abolished by prior intrarenal infusion of prazosin (0.5 μg/kg/min for 30 min). In separate groups of experiments, the animals received either a selective irreversible α 1A-adrenoceptor antagonist, SZL-49 [1-(4-amino-6,7-dimethoxy-2-quinazolinyl)-4-(2-bicyclo[2,2,2]octa-2,5-diene-2-carbonyl)piperazine], or an α 1B-adrenoceptor antagonist, chloroethylclonidine, intrarenally prior to phenylephrine infusion. Neither SZL-49 nor chloroethylclonidine alone significantly altered glomerular filtration rate and renal electrolyte excretion. However, SZL-49 (0.15 μg/kg/min), but not chloroethylclonidine (50 μg/kg/min), completely abolished phenylephrine-induced changes in urine output, Na + excretion and glomerular filtration rate. These results demonstrate that phenylephrine decreases urine output and Na + excretion, mainly due to a reduction in glomerular filtration rate resulting from activation of α 1A-adrenoceptors, and that proximal tubular α 1A- or α 1B-adrenoceptors do not appear to contribute to this response.

OPIOID MECHANISMS CONTROLLING RENAL FUNCTION

1. Over the past 50 years considerable evidence has been reported suggesting that endogenous opioids participate in the control of renal function. 2. Exogenous administration of opioids produces profound changes in the renal excretion of water and sodium. 3. Opioids produce changes in urine output and urine sodium excretion by multiple integrated neural and hormonal mechanisms within the periphery, central nervous system and kidneys. 4. Although opioid antagonist administration does not consistently reveal an action of endogenous opioid systems on renal function, this may result from the quiescent nature of the endogenous opioid system under basal conditions. 5. Manipulations that activate endogenous opioid systems have begun to reveal important, previously unrecognized mechanisms that control kidney function and can enhance renal tubular sodium reabsorption in normal and potentially pathological states.

Renal support in critically ill patients: Low-dose dopamine or low-dose dobutamine?

Low-dose dopamine has been used in critically ill patients to minimize renal dysfunction without sufficient data to support its use. The aim of this study was to determine whether low-dose dopamine improves renal function, and whether dobutamine, a nondopaminergic inotrope, improves renal function. Prospective, randomized, double-blind trial. Twenty-three patients at risk for renal dysfunction were entered into the study. Five patients were later withdrawn. Study data for the remaining 18 patients were: mean age 55 yrs; mean Acute Physiology and Chronic Health Evaluation (APACHE) II score of 18; mean weight 71 kg). The following conditions were present: mechanical ventilation (n = 17 [inverse-ratio ventilation, n = 6]); inotrope administration (n = 11); sepsis (n = 13); and adult respiratory distress syndrome or multiple organ failure syndrome (n = 9). The study patients were administered dopamine (200 micrograms/min), dobutamine (175 micrograms/min), and placebo (5% dextrose) over 5 hrs each in a randomized order. Ventilator settings, fluid management, and preexisting inotropic support were not altered during the study. Systemic hemodynamic values and indices of renal function (4-hr urine volume, fractional excretion of sodium, and creatinine clearance) were measured during the last 4 hrs of each infusion. Dopamine produced a diuresis (145 +/- 148 mL/hr) compared with placebo (90 +/- 44 mL/hr; p < .01) without a change in creatinine clearance. Conversely, dobutamine caused a significant increase in creatinine clearance (97 +/- 54 mL/min) compared with placebo (79 +/- 38 mL/min; p < .01), without an increase in urine output. In stable critically ill patients, dopamine acted primarily as a diuretic and did not improve creatinine clearance. Dobutamine improved creatinine clearance without a significant change in urine output.

Attenuation of adenylate cyclase-induced increases in renal sodium excretion by the dopamine D-2 receptor agonist SK&F 89124.

1. Although the existence of D-2 receptor binding sites in kidney has been identified, their functional significance in terms of influencing renal sodium excretion is not clear. In the present study we have examined the renal effects of a selective D-2 receptor agonist, SK&F 89124, in anaesthetized rats. 2. Intravenous infusion of SK&F 89124 (0.3, 1 and 3 micrograms kg-1 min-1 respectively) produced dose-dependent decreases in mean arterial blood pressure, heart rate and renal blood flow without causing any significant changes in urine output, urinary sodium excretion, renal vascular resistance or glomerular filtration rate. The changes in blood pressure, heart rate and renal blood flow caused by SK&F 89124 were abolished by a selective D-2 receptor antagonist, domperidone (50 micrograms kg-1 i.v. bolus; 10 micrograms kg-1 min-1). 3; Treatment with 3-isobutyl-1-methylxanthine (IBMX, 1 mg kg-1 bolus i.v.) or forskolin (200 micrograms kg-1 bolus i.v.) produced increases in heart rate, urine output and urinary sodium excretion, but there was no change in mean blood pressure. The natriuretic and diuretic response, but not tachycardiac response to IBMX or forskolin, was attenuated by SK&F 89124 (0.3 micrograms kg-1 min-1). 4. These results suggest that the selective D-2 receptor agonist, SK&F 89124, produced a significant decrease in blood pressure and heart rate via prejunctional D-2 receptor-mediated inhibition of noradrenaline release from postganglionic sympathetic nerve terminals. Although activation of renal tubular D-2 receptors had no significant effect on renal excretory function under basal conditions, it is likely that these receptors may exert an opposing effect on cAMP-mediated increases in renal sodium and water excretion.

Renal afferents signaling diuretic activity in the cat.

Mechanoreceptors and chemoreceptors have been identified inside the kidney, but their functional role is still largely unclear. The aim of this study was to investigate whether changes in urine output could modify the discharge rate of renal afferent fibers. Experiments were performed in anesthetized cats in which afferent renal nerve activity (ARNA) was recorded by standard electrophysiological techniques from a centrally cut renal nerve. Arterial pressure, renal blood flow velocity, urine flow rate, and renal pelvic pressure were also measured. Three diuretic maneuvers were tested in the same cat: intravenous administration of physiological saline (8 to 13 mL/min for 2 minutes), furosemide (1 mg/kg), and atrial natriuretic peptide (ANP, 1 microgram/kg). The three maneuvers increased urine flow rate and pelvic pressure, respectively, 137.0 +/- 20.6% and 136.8 +/- 21.1% (saline), 148.6 +/- 31.7% and 139.6 +/- 43.5% (furosemide), and 75.9 +/- 7.9% and 62.1 +/- 21.2% (ANP) at the time of the maximum response. Arterial pressure slightly increased after saline, did not change after furosemide, and slightly decreased after ANP. Renal blood flow increased after saline and did not change after furosemide and ANP. The three maneuvers increased ARNA by 98.4 +/- 15.2% (saline), 270.7 +/- 100.8% (furosemide), and 59.6 +/- 23.4% (ANP). Changes in ARNA significantly correlate with changes in both pelvic pressure and urine flow rate. Our data demonstrate that increments in urine flow rate increase the firing rate of renal afferent fibers and suggest that (1) pelvic pressure is the major determinant of the neural response, and (2) this increased afferent discharge is due to activation of renal mechanoreceptors.

Renal complications of nonsteroidal anti-inflammatory drugs

A 63-year-old, hypertensive, nondiabetic man with a 4-year history of gout was hospitalized because of painful swelling of his right foot. His blood pressure had been treated with nifedipine, 20 mg orally, three times daily. On admission, the patient was normotensive (blood pressure, 140/85 mm Hg) and had no clinical signs of congestive heart failure or volume depletion. Physical examination revealed erythema and soft-tissue swelling of the dorsum of the right foot with metatarsal tenderness. Laboratory data showed mild azotemia with a BUN level of 23 mg/dl; serum creatinine, 1.8 mg/dl; creatinine clearance, 70 mllmin; serum potassium, 4.1 mEq/liter; serum bicarbonate, 24 mmol/liter; and serum uric acid, 13.2 mg/dl. Roentgenographic findings were consistent with erosive gout, and a diagnosis of acute gouty attack was made. Indomethacin, 50 mg orally three times daily, was begun. The patient's symptoms improved rapidly, but within 4 days, the BUN rose to 51 mg/dl; serum creatinine, 2.4 mg/dl; serum potassium, 6.6 mEq/liter; and serum bicarbonate, 27 mmollliter; the creatinine clearance decreased to 36 mI/mm, with a fractional excretion of sodium of 0.06% and a urinary potassium concentration of 21 mEq/liter. The urinary sediment was unremarkable. The patient's blood pressure ranged from 140/85 to 150/90 mm Hg and no major changes in urinary output were noted. Indomethacin treatment was discontinued and replaced by colchicine. The patient's renal function and serum potassium level returned to baseline values within 4 days.

Ureteric jets: evaluation of normal flow dynamics with color Doppler sonography.

This study was designed to investigate a variety of sonographic features of ureteric jets in order to define patterns of flow and ranges of flow values in an asymptomatic population. The following features of ureteric jets were measured during a period of up to 30 min in a group of 15 asymptomatic volunteers after oral hydration (the mean value was calculated on each side): peak velocity (mean, 57 cm/sec); jet duration (mean, 4.6 sec); and number of peaks and subpeaks (mean, 2.2). Several flow patterns were observed, including discrete jets, ureteric streaming, and rest periods. For each patient the ratios of values obtained on the left and right sides were calculated for peak velocity (1.00-1.74; mean, 1.26); jet duration (1.00-4.69; mean, 1.83); and jet frequency (1.00-1.21; mean, 1.11). The interjet interval (period between jets) ranged from 2 to 150 sec. Bolus volume and jet frequency showed simultaneous moment-to-moment variation. The frequency and velocity rather than the duration ratios may be of greatest value in identifying patients with normal ureterodynamics. Our findings challenge two current concepts of renal pelvic and ureteral response to changes in urine output: (1) ureters have a fixed maximal discharge rate and (2) bolus volumes do not change until this rate is achieved. Asymmetric moment-to-moment fluctuations observed in jet frequency suggest that prolonged examination may be necessary to confirm normal symmetry of jet frequency in some patients with suspected ureteric obstruction.

Effect of induced supraventricular tachycardias on changes in urine output and plasma hormone levels in man.

1. A symptomatic diuresis, polyuria, sometimes accompanies paroxysmal tachycardias in man. A study was undertaken in patients with inducible supraventricular tachycardia, irrespective of the symptom of polyuria, to measure simultaneous changes in urine output and plasma hormone levels during the arrhythmia. 2. During 14 episodes of induced tachycardia in 10 patients, there was a significant increase in mean urine flow, which was independent of the state of patient hydration. During a mean tachycardia duration of 30 +/- 3 min, the mean group urine flow increased from 3.2 +/- 2.3 ml/min to 7.6 +/- 3.7 ml/min (P less than 0.001). This was characterized by a consistent increase in free water excretion and a variable increase in sodium excretion. 3. The plasma atrial natriuretic peptide level (five patients) significantly increased from 7.6 +/- 4.6 pg/ml to 34.6 +/- 21.7 pg/ml (P less than 0.02) during the arrhythmia. There was no significant change in the plasma arginine-vasopressin level and a non-significant reduction in plasma renin activity. 4. This study has shown that induced supraventricular tachycardias in man are accompanied by a significant diuresis. The mechanisms responsible remain unknown, but do not appear to involve the plasma arginine-vasopressin level alone.