The acute natriuretic response to atrial peptides (AP) is highly variable in anesthetized rats, and some rats are unresponsive. To determine if this response to AP was affected by dehydration, we measured hematocrit, plasma volume, and natriuresis (delta UNaV) after intravenous injection of 3 micrograms/kg of rat atriopeptin III (rAPIII) in anesthetized rats deprived of water for 0, 12, 20, 29, 44, and 68 hours. Data were compared with those from rats receiving 1.5 mg/kg furosemide (FU) after 0 and 68 hours without water. There were 10- and 3-fold decreases in delta UNaV following rAPIII and FU injection after 20 and 68 hours without water, respectively. Hematocrit increased and plasma and total blood volumes decreased after 12 hours of dehydration. Plasma volumes and delta UNaV were correlated (r = 0.64, p less than 0.05; r = 0.75, p less than 0.001) in the combined groups receiving rAPIII (n = 30) and FU (n = 10), respectively. These results demonstrate that a relatively short period of water deprivation (WD) and the resulting hemoconcentration in rats decreased their acute natriuretic response to diuretics. Thus, differences in water intake may account for some of the large variation in delta UNaV after exogenous administration of rAPIII.
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Renal tubular acidosis is a syndrome of disordered renal acidification, we have studied a group of patients transplanted. Their cases clinic patients have been analyzed with no-present infectious disease, or tubulointerstitial diseases or urinary infection, immunosuppression with prednisone and azatioprine only, no have to ingest cyclosporine and period graft superior 3 months. We haven't neither patient with proximal renal tubular acidosis. We have been reported 7 cases of distal renal tubular acidosis. All the patients have make the furosemide test. Only one case hyperkalemia renal tubular acidosis. Histologic kidney had been chronic rejection.
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We present a 30-year-old man with nephrotic syndrome presenting with bilateral perirenal massive collection compatible with transudation. After drainage of collections kidney biopsy was performed and the histologic diagnosis was focal and segmental glomerulosclerosis. The patient was treated with cyclophosphamide, prednisone, furosemide and enalapril. After remission of nephrotic syndrome renal ultrasound showed complete resolution of perirenal collections. In conclusion, the case shows that perirenal subcapsular transudation is a rare complication of nephrotic syndrome and massive collections can be treated successfully by percutaneous drainage.
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Removal of chloride (Cl-) from the superfusion medium results in increased spontaneous efflux of dopamine (DA) but not acetylcholine from rabbit striatal slices prelabeled with [3H]DA and [14C]choline. Cl- was substituted to varying degrees with the impermeant anion, isethionate (IS-), or the permeant anion, nitrate (NO3-). The magnitude of low Cl(-)-induced DA efflux was inversely related to the external [Cl-] and was greater with IS- than with NO3-. Analysis of the composition of the 3H efflux in terms of DA and its metabolites revealed an increase in [3H]DA with decreasing Cl- concentration. Reduction of external Ca++ from 1.3 to 0.13 mM increased low Cl(-)-induced DA efflux. In slices depleted of vesicular DA by reserpine pretreatment and subsequently labeled and superfused in the presence of monoamine oxidase and catechol-O-methyltransferase inhibitors, the same inverse relationship between [Cl-] and spontaneous DA efflux was observed. Neuronal DA uptake inhibitors, nomifensine, mazindol, GBR-12909 and cocaine, all increased the rate of low Cl(-)-induced DA efflux in the reserpinized preparation. Cl(-)-induced DA efflux in untreated and reserpinized preparations was not blocked by tetrodotoxin, amiloride, furosemide, picrotoxin or 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid). Low Cl- inhibited initial rates of [3H]DA uptake. At Cl- concentrations producing significantly different efflux rates (0 and 7.4 mM Cl-, IS- and NO3- substitution), DA uptake was inhibited in all cases by greater than 90%. Additionally, the binding of [3H]mazindol, one of the uptake inhibitors, to striatal membranes was unaffected by removal of Cl-. In summary, low Cl- produces a nonexocytotic rapid outward transport of DA. Extracellular Cl- is not required for the binding to transporter sites or for the inhibition of neuronal uptake produced by neuronal uptake inhibitors.
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At the time of catheterization, dyspnoea class III or IV was present in 60% of the patients, atrial fibrillation in 19% and complete left bundle branch block in 35%. Left ventricular ejection fraction was 30 +/- 10% and right ventricular ejection fraction was 30 +/- 16%. During follow-up (2.2 +/- 1.3 years), 15 patients (24%) had heart transplantation and nine (14%) died before cardiac transplantation. Cumulative survival rate without heart transplantation was 74% and 56% at 1 and 4 years, respectively. In univariate analysis, survival was related to: dyspnoea class I or II (P < 0.04), absence of complete left bundle branch block (P < 0.05), administration of lower doses of furosemide (P < 0.01), high left ventricular ejection fraction (P < 0.001), low pulmonary artery pressure (P < 0.002), high cardiac index (P < 0.006), and low right ventricular volumes (P < 0.001). Multivariate analysis showed only two independent predictors of survival: left ventricular ejection fraction (P < 0.001) and right ventricular ejection fraction (P < 0.004).
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Our objective was to determine whether cardiac surgery patients receiving therapy with potassium-wasting diuretics can safely and beneficially maintain serum potassium levels by eating potassium-rich foods.
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Here, we studied the effect of these drugs on [(14)C]urate transport using human embryonic kidney 293 cells overexpressing human MRP4 and in membrane vesicles isolated from these cells.
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AHF is a major public health problem in Botswana, with high in-hospital and post-discharge mortality rates and prolonged hospital stays. Late and symptomatic presentation is common, and the most common aetiologies are preventable and/or treatable co-morbidities, including hypertension, diabetes mellitus, renal failure and HIV.
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Perioperative death occurred in two patients (5.9%) due to cardiogenic shock complicating acute myocardial infarction. Perioperative cardiac morbidity occurred in 16 patients (47.1%); noncardiac morbidity was seen in 12 patients (35.3%). Preoperative unstable angina was the only variable predictive of perioperative death (p = 0.005). Cardiac (p = 0.005) and noncardiac (p < 0.001) morbidity rates were significantly higher for the initial 15 patients undergoing the procedure. Other predictors of perioperative complications included lack of postoperative treatment with a furosemide infusion (p < or = 0.04) and preoperative unstable angina (p = 0.05).
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The literature is reviewed and the arguments in favor of expectant observation versus early operation are discussed.
The groups were similar for age, sex, EF, risk factors, treatment and etiology of CHF. All patients showed a clinical improvement. Six patients in both groups had hyponatremia (from 120 to 128 mEq./l) at entry. A significant increase in daily diuresis in both groups was observed (from 390+/-155 to 2100+/-626, and from 433+/-141 to 1650+/-537 ml/24 h, P<0.05). Natriuresis (from 49+/-15 to 198+/-28 mEq./24 h) was higher in group 1 vs. group 2 (from 53.83+/-12 to 129+/-39 mEq./24 h, P<0.05). Serum Na (from 135.9+/-6.8 to 142.2+/-3. 8 mEq./l, P<0.05) increased in the group 1 and decreased in the group 2 (from 134.7+/-7.9 to 130.1+/-4.3 mEq./l). Serum K was decreased (from 4.4+/-0.6 to 3.9+/-0.6, and 4.6+/-9 to 3.6+/-0.5 mEq. /l, P<0. 05) in both groups. BW was reduced (from 73.8+/-9.1 to 63. 8+/-8.8, and from 72.9+/-10.2 to 64.5+/-7.5 kg, P<0. 05) in both groups. Group 2 showed more patients in NYHA class III than group 1 (18 vs. 2 patients, P<0.05). Group 2 showed an increase of serum creatinine. Serum uric acid increased in both groups. BP values decreased, and HR was corrected to normal values in both groups. Group 2 showed a longer hospitalization time than group receiving HHS infusion (11.67+/-1.8 vs. 8.57+/-2.3 days, P<0.001). In the follow-up (6-12 months), none of the patients from group 1 were readmitted to the hospital and they maintained the NYHA class achieved at the discharge. Group 2 showed 12 patients readmitted to hospital and a higher class than at discharge.
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Epimastigotes grew significantly more slowly in 2mM than in 50mM Pi. Influx of Pi into parasites grown under low Pi conditions took place in the absence and presence of Na(+). We found that the parasites express TcPho84, a H(+):Pi-symporter, and TcPho89, a Na(+):Pi-symporter. Both Pi influx mechanisms showed Michaelis-Menten kinetics, with a one-order of magnitude higher affinity for the Na(+)-dependent system. Collapsing the membrane potential with carbonylcyanide-p-trifluoromethoxyphenylhydrazone strongly impaired the influx of Pi. Valinomycin (K(+) ionophore) or SCH28028 (inhibitor of (H(+)+K(+))ATPase) significantly inhibited Pi uptake, indicating that an inwardly-directed H(+) gradient energizes uphill Pi entry and that K(+) recycling plays a key role in Pi influx. Furosemide, an inhibitor of the ouabain-insensitive Na(+)-ATPase, decreased only the Na(+)-dependent Pi uptake, indicating that this Na(+) pump generates the Na(+) gradient utilized by the symporter. Trypomastigote forms take up Pi inefficiently.
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Long term diuretic therapy represents one central pharmacologic therapy of heart insufficiency and hypertension. Diuretics lead not only to an increased urinary excretion of electrolytes but also of water soluble vitamins. In this prospective study we evaluated the effect of hospitalization on the overall biochemical vitamin status in subjects older than 50 years (n=149, mean +/- SD age 70 +/- 10 years). Vitamin nutriture and other parameters were assessed at admission and discharge (duration of the hospitalization 19 +/- 1 day). Only vitamin B1 nutriture worsened during the hospitalization and in a multivariate procedure the only significant predictor of the change in the vitamin B1 nutriture was the use of diuretics during the hospitalization (F=4.06, p < 0.001). The changes in the ETK (erythrocyte transketolase activity in whole blood) and a-ETK (ETK activity coefficient) during the hospital stay correlated with the cumulative dosage of furosemide adjusted for the duration of the therapy (r = 0.36, p < 0.001 and r = - 0.28, p > 0.03). Our data suggest that hospitalized elderly are at increased risk for vitamin B1 deficiency especially when on a diuretic treatment. It is possible that a low dose thiamine supplementation my help to prevent the development of a subclinical wet-beriberi in older subjects on diuretics.
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Mean age was 64.9 years (SD = 9.7, range 41 - 84 years); 76.3% (119) were male. The in-hospital mortality was 1.2% (2 patients). The incidence of AF was 32.1% (50), with 40% of the AF episodes occurring on the second postoperative day (range 1-6 days). Univariate analyses identified the following variables as risk factors for AF: female gender, older age, ethnic origin, BMI > 30, hypertension, dyslipidemia, pre CABG nitrate, Ca blockers and furosemide treatment, left atrial diameter, renal failure and post CABG respiratory complications (p <0.05). By multivariate analysis, three variables were identified as independent predictors: BMI>30 (odds ratio 2.4; 95% CI 1.2-4.8); Sephardic Jews (OR 11.2; CI 1.0-114); enlarged left atrium (OR 4.6; CI 1.5-14.1).
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In order to evaluate the relevance of in vitro methods for immunotoxicity assessment, the effects of pharmaceutical drugs on lymphoproliferative and cytotoxic functions of mouse splenocytes and human peripheral blood mononuclear cells (hPBMC) were studied. A comparison of sensitivity of immune cells from different origins to an in vitro exposure to different xenobiotics was performed using non-immunosuppressive (cimetidine and furosemide) and immunosuppressive (azathioprine (AZA), cyclosporine A (CSA), and dexamethasone (DEX)) drugs. For CSA, sensitivity of both rat and mouse splenocytes following in vitro exposure was compared to the one of hPBMC. Immune function tests included lymphoproliferative response to mitogenic lectins (concanavalin A (Con A) and phytohemagglutinin (PHA-P)) or to allogeneic cells (mixed leukocyte response (MLR)) and cytotoxicity assays (cytotoxic-T lymphocyte (CTL) and natural killer (NK) cell-mediated cytolysis). Additionally, to evaluate how well in vitro assays represent the in vivo situation, a comparison of the effect of cyclosporine A on the same immune function tests following in vivo or in vitro exposure was performed. The data obtained show numerous similarities in the effects observed following in vitro exposure of rodent or human cells to the drugs and a very similar sensitivity of rat and mouse cells to CSA in vitro. Discrepancies between human and rodent cells such as lymphoproliferative response to PHA-P following exposure to DEX or sensitivity of CTL-mediated cytolysis to CSA do exist. In vitro assays were very representative of the in vivo situation, both in the rat and in the mouse, following CSA exposure, except for NK cell activity in the rat. These data show the usefulness of in vitro systems for immunotoxicity assessment. They allow direct comparison of rodent and human systems, and could be representative, for drugs altering specifically the immune system like CSA does, of the in vivo situation.
1. Suspending human red blood cells in isotonic sucrose (low ionic strength, LIS) medium induces a significant increase in membrane transport of glutamine, glutamate, lactate, histidine, taurine, glycine, serine, choline and carnitine but not sorbitol or sucrose. 2. Progressive lowering of ionic strength by sucrose or NaCl replacement gave a similar activation profile for taurine influx as found earlier for residual K+(86Rb+) flux. 3. The induced taurine transport could be measured as enhanced influx and efflux. Influx was linear with external concentration up to 10 mM, largely insensitive to alteration in cell volume, and did not vary with red blood cell age. 4. Unlike previous results for residual K+ transport, altering transmembrane potential with gluconate or glucuronate media led to an increase in taurine influx similar to that observed in LIS media. Varying medium pH confirmed the effect was not due to alteration in pH. 5. The LIS-induced flux was sensitive to a variety of 'classical' anion transport inhibitors in the order of potency DNDS, DIDS, NPPB, DIOA, niflumic acid, furosemide (frusemide), glibenclamide, nitrendipine and bumetanide. 6. The taurine flux showed a temperature dependence similar to that of the LIS-induced residual K+ flux. High hydrostatic pressure (40 MPa), however, inhibited taurine flux but stimulated residual K+ influx in LIS media. 7. A significant enhanced taurine flux could be demonstrated in red blood cells of other species, including horse, cattle, pig and high and low potassium type sheep. 8. It is concluded that lowering ionic strength activates a transport pathway for organic molecules sharing some similarities with background Cl- channels and LIS-induced residual K+ fluxes. In the latter context, however, there are certain significant differences (effect of transmembrane potential; volume; pressure sensitivity; species distribution) which may be important, and the unequivocal identity of the two transport processes remains to be confirmed.
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Prostaglandins (PGs) can modulate a variety of renal functions, including Na+ and Cl- reabsorption. However, it is not known if a direct interdependence exists between PG synthesis and transport activity. The present study was done to find out whether or not the rate of NaCl transport has an influence on PG synthesis in renal tubular cells. For our studies we used cultures of so-called high-resistance MDCK cells, which were originally derived from canine kidney. This cell type has a loop diuretic- and ouabain-sensitive NaCl transport that can be enhanced by activation of the adenylate cyclase (AC). In MDCK cell cultures we found that each state of increased NaCl transport during stimulation of AC by either epinephrine (10(-6) M), isoprenaline (10(-5) M), or forskolin (10(-5) M) was accompanied by a twofold increase in PG release. During inhibition of NaCl transport by furosemide (10(-4) M) or ouabain (2 X 10(-4) M), stimulation of AC failed to increase PGE2 release, whereas basal PG production was not inhibited by either furosemide or ouabain. Furthermore, PG formation during activation of AC was dependent on the concentration of extracellular Na+, whereas PG formation in the absence of activators of AC was independent of extracellular Na+. These results suggest that increased NaCl transport stimulates PG formation in cultures of high-resistance MDCK cells.
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The average operative time was 60 minutes. Mean hospital stay was 48 hours. There were no complications during the procedure. In five patients urinary infection episodes disappeared. Ultrasound demonstrated decreased hydronephrosis and megaureter. In two patients the differential renal function following the technique improved. One patient with preoperative split renal function of 14% required nephrectomy. One patient had postoperative vesicoureteral reflux.
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We present a case of a 60-year-old Caucasian woman, with no prior history of swellings, who was admitted to a hospital due to life-threatening angio-oedema. She had, the previous day, been prescribed an ACE inhibitor for her essential hypertension. She had taken one tablet at night-time, and awoke in the morning with a swollen face progressing to involve the tongue and throat within a few hours. On arrival at her doctor's office, her voice had altered. Corticosteroids and antihistamine were administered while awaiting an ambulance. Arriving at the emergency department, she had dyspnoea due to increasingly severe angio-oedema of the upper airways. Neither adrenaline inhalations, intravenously administrated corticosteroids, atropine nor furosemide were effective and the patient soon become bradycardic. A tracheotomy was performed and the patient was placed on a ventilator. She eventually made a full recovery. It was concluded that she had suffered from life-threatening angio-oedema due to her new medication.
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High-resolution real-time ultrasonography (US) serves as an important tool for differentiation of obstructive and nonobstructive causes of jaundice in infants and children, independent of liver function. Unconjugated hyperbilirubinemia occurs in approximately 60% of normal term infants and in 80% of preterm infants. Persistence of neonatal jaundice beyond 2 weeks of age demands US evaluation to differentiate between the three most common causes: hepatitis, biliary atresia, and choledochal cyst. In all three conditions, the hepatic echotexture is diffusely coarse and hyperechoic, but this appearance may be seen in a variety of hepatic inflammatory, obstructive, and metabolic processes. Thus, hepatic scintigraphy and at times percutaneous liver biopsy are necessary to narrow the differential diagnosis and to identify patients who require more invasive techniques (eg, intraoperative cholangiography). US is useful for demonstrating inspissated bile and biliary duct stones. In infants, stones are usually secondary to obstructive congenital anomalies of the biliary tract, total parenteral nutrition, furosemide treatment, phototherapy, dehydration, infection, hemolytic anemia, and short-gut syndrome, whereas in older children, stones are usually associated with sickle cell disease, bowel resection, hemolytic anemia, and choledochal cyst. Jaundice in infants and children may also be due to cirrhosis, benign strictures, and neoplastic processes.
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This study was approved by our Institutional Animal Care and Use Committee. Four water-restricted pigs were CT-scanned at 80 and 140 kVp at baseline and at 5 min intervals for 30 min during saline or furosemide diuresis. The renal cortical and medullary CT numbers were recorded. A DECT basis material decomposition method was used to quantify renal cortical and medullary sodium concentrations and medulla-to-cortex sodium ratios at each time point based on the measured CT numbers. The sodium concentrations and medulla-to-cortex sodium ratios were compared between baseline and at 30 min diuresis using paired Student t-tests. The medulla-to-cortex sodium ratios were considered to reflect the corticomedullary sodium gradient.
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In addition to blocking cyclooxygenases, members of the fenamate group of nonsteroidal anti-inflammatory drugs have been proposed to affect brain GABAA receptors. Using quantitative autoradiography with GABAA receptor-associated ionophore ligand [35S]t-butylbicyclophosphorothionate (TBPS) on rat brain sections, one of the fenamates, niflumate, at micromolar concentration was found to potentiate GABA actions in most brain areas, whereas being in the cerebellar granule cell layer an efficient antagonist similar to furosemide. With recombinant GABAA receptors expressed in Xenopus laevis oocytes, we found that niflumate potentiated 3 microM GABA responses up to 160% and shifted the GABA concentration-response curve to the left in alpha1beta2gamma2 receptors, the predominant GABAA receptor subtype in the brain. This effect needed the gamma2 subunit, because on alpha1beta2 receptors, niflumate exhibited solely an antagonistic effect at high concentrations. The potentiation was not abolished by the specific benzodiazepine site antagonist flumazenil. Niflumate acted as a potent antagonist of alpha6beta2 receptors (with or without gamma2 subunit) and of alphaXbeta2gamma2 receptors containing a chimeric alpha1 to alpha6 subunit, which suggests that niflumate antagonism is dependent on the same transmembrane domain 1- and 2-including fragment of the alpha6 subunit as furosemide antagonism. This antagonism was noncompetitive because the maximal GABA response, but not the potency, was reduced by niflumate. These data show receptor subtype-dependent positive and negative modulatory actions of niflumate on GABAA receptors at clinically relevant concentrations, and they suggest the existence of a novel positive modulatory site on alpha1beta2gamma2 receptors that is dependent on the gamma2 subunit but not associated with the benzodiazepine binding site.
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2,4,7-Triamino-6-(4-methanesulfonamidophenyl) pteridine (RPH 3048) is a new acidic triamterene derivative. Relevant physico-chemical constants were determined (solubility at pH 7.4 = 3.7 mg/l; logP at pH 7.4 = 0.2) and pharmacokinetic as well as pharmacodynamic properties were investigated, using male Wistar rats. After intravenous application of the test substances urine was collected, its volume and electrolyte composition determined, and the urine recovery of the drugs was analysed. The comparison of RPH 3048 with triamterene (CAS 396-01-0) revealed almost equipotent natriuretic and potassium-retaining effects for both drugs and an additional relative magnesium-sparing activity of RPH 3048. The urine recovery of RPH 3048 after 6 h was higher (20.6%) than that of triamterene (12.9%). No metabolite of RPH 3048 could be detected in the urine whereas a triamterene metabolite was found. Due to its good solubility in alkaline medium RPH 3048 could be dissolved (at pH 11-12) and then administered intravenously together with a loop diuretic (furosemide). Urinary electrolyte excretion following administration of two different combinations of RPH 3048 and furosemide (combination A: 12.5 mumol/kg RPH 3048 and 25 mumol/kg furosemide; combination B: 25 mumol/kg RPH 3048 and 25 mumol/kg furosemide) was compared to urinary electrolyte excretion of a control group and a group only treated with furosemide (25 mumol/kg). The additional application of RPH 3048 reduced in both groups potassium and magnesium excretion to control level but did not compromise furosemide induced natriuresis. In contrast to earlier investigations these results suggest that it is possible to develop acidic triamterene derivatives with potent antikaliuretic effects.
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Symptoms in patients varied from mild (muscle weakness and numbness) to severe (tetany and foot paralysis). All patients were normotensive or hypotensive, and all had hypokalaemia, hypocalciuria, and hyperreninaemic hyperaldosteronism. However, two male patients had normomagnesaemia, while the remainder was hypomagnesaemic. Renal clearance tests showed that the administration of furosemide decreased distal fractional chloride reabsorption, while thiazide ingestion failed to decrease it. Genetic analysis identified six thiazide-sensitive Na-Cl co-transporter gene mutations, including two novel ones. Therefore, on the basis of the confirmatory renal clearance tests and mutational analysis, a diagnosis of Gitelman's syndrome was made in these patients.
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It is understood that dilation per se does not mean obstruction but, if all other parameters indicate obstruction, we recommend early surgical treatment to prevent obstructive damage to the immature infant kidney and because better recovery of function is possible when surgery is done in the first year of life.
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Renal effects of a selective cyclooxygenase-2 (COX-2) inhibitor [MF-Tricyclic; 3-(3,4-difluorophenyl)-4-(4-(methylsulfonyl)phenyl)-2-(5H)-furanone] were studied in control and volume-depleted conscious dogs. MF-Tricyclic was compared with the nonselective COX-1/COX-2 inhibitor indomethacin. Six instrumented male dogs were randomly selected to receive MF-Tricyclic or indomethacin at 10 mg/kg. Volume depletion was effected by a sodium-restricted diet (14 days) with administration of furosemide (7.5 mg/kg, i.v.) the day before the experiment. Indomethacin ablated systemic COX-1 activity (p < 0.05), whereas MF-Tricyclic did not affect this activity. Each compound achieved plasma concentrations in excess of their respective median inhibitory concentrations (IC50 values) against canine COX-2. In controls, neither compound affected mean arterial pressure (MAP), heart rate (HR), renal blood flow (RBF), fractional excretion (FE) Na+, or FE K+. In volume-depleted dogs, indomethacin reduced RBF (p < 0.05), whereas MF-Tricyclic did not affect this parameter. Indices of renal function in volume-depleted dogs were not affected. These data are consistent with the view that the effects of indomethacin on RBF are a consequence of inhibition of COX-1 activity. Furthermore, in these studies, short-term administration of a selective COX-2 inhibitor was without deleterious effects on renal function.
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Intravenous bolus administration of 30 mL of 23.4% saline.