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Preliminary results demonstrate a good feasibility of furosemide-enhanced MS-CTU for obtaining detailed visualization of the entire upper urinary tract.
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To evaluate the feasibility and efficacy of robotic-assisted laparoscopic pyeloplasty. Laparoscopic pyeloplasty has been shown to have a success rate comparable to that of the open surgical approach. However, the steep learning curve has hindered its acceptance into mainstream urologic practice. The introduction of robotic assistance provides advantages that have the potential to facilitate precise dissection and intracorporeal suturing.
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Human carbonic anhydrase II (CA II), a zinc metalloenzyme, was screened against 960 structurally diverse, biologically active small molecules. The assay monitored CA II esterase activity against the substrate 4-nitrophenyl acetate in a format allowing high-throughput screening. The assay proved to be robust and reproducible with a hit rate of approximately 2%. Potential hits were further characterized by determining their IC(50) and K(d) values and tested for nonspecific, promiscuous inhibition. Three known sulfonamide CA inhibitors were identified: acetazolamide, methazolamide, and celecoxib. Other hits were also found, including diuretics and antibiotics not previously identified as CA inhibitors, for example, furosemide and halazone. These results confirm that many sulfonamide drugs have CA inhibitory properties but also that not all sulfonamides are CA inhibitors. Thus many, but not all, sulfonamide drugs appear to interact with CA II and may target other CA isozymes. The screen also yielded several novel classes of nonsulfonamide inhibitors, including merbromin, thioxolone, and tannic acid. Although these compounds may function by some nonspecific mechanism (merbromin and tannic acid), at least 1 (thioxolone) appears to represent a genuine CA inhibitor. Thus, this study yielded a number of potentially new classes of CA inhibitors and preliminary experiments to characterize their mechanism of action.
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The dynamic range in which renal blood flow (RBF) autoregulation occurs was determined in eight conscious foxhounds chronically catheterized in the abdominal aorta and implanted with a transit-time flow probe over the renal artery. Sinusoidal driving pressures (amplitude of 10 mmHg) were forced on the renal arterial pressure at different frequencies by a servo-control device, and transfer functions were calculated. Only one frequency range was found below which the gain of the transfer function declined and in which the phase angle increased (n = 8). This indicates the presence of a potent mechanism for renal autoregulation in the examined frequency range between 0.0031 and 0.08 Hz, which buffers changes in blood flow < 0.02 Hz. After furosemide treatment, one indicator for autoregulation (phase shift of transfer function) was significantly blunted at low frequencies (n = 6). Furosemide, however, did not reduce the phase shift to zero, suggesting that some autoregulation still remained in the frequency range between 0.04 and 0.08 Hz. In conclusion, autoregulation of RBF during sinusoidal changes in driving pressure between 0.0031 and 0.02 Hz is mediated by a single mechanism, which can be blocked by the acute administration of furosemide. The residual phase shift between arterial pressure and RBF in the transfer function observed during sinusoidal changes in driving pressure between 0.04 and 0.08 Hz suggests the presence of a second mechanism for RBF autoregulation.
Loop diuretics are prescribed commonly, particularly in the elderly. There is no clear pattern of documented clinical features that leads to prescription of these drugs. Open access echocardiography is rarely used to aid diagnosis. ACE inhibitors are under-prescribed and under-dosed in patients diagnosed with heart failure in this study population.
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A 35-year-old man, a heavy smoker, was admitted to the hospital because of lobar pneumonia. Despite wide spectrum antimicrobial therapy, he developed ARDS and was placed on a ventilator. Standard ventilation was ineffective and veno-venous ECMO was instituted. The extravascular lung water index (EVLWI) was extremely high (over 30 mL kg-1) and signs of a hyperdynamic circulation (CI 6.1 L m-2 min-1) were observed. Modification of the inotropic support and continuous infusion of furosemide resulted in normalisation of the hydration status, and over a week of ECMO therapy, the patient's general condition improved to the stage that he was scheduled to be weaned from extracorporeal treatment. On the 7th day however, he suddenly deteriorated. A lung CT-scan revealed bilateral pneumothoraces and diffuse pulmonary embolism. Three thoracic drains were inserted, but unfortunately, the drainage was complicated by massive bleeding and a subsequent thoracotomy. Two days later, a gastrointestinal haemorrhage occurred. Heparin dosage was reduced, and ECMO was discontinued and replaced with HFOV. This resulted in adequate oxygenation, however because of ineffective CO2 elimination, pumpless arteriovenous extracorporeal lung assist (PECLA) was instituted, allowing conventional ventilation to be resumed after 8 days. The further clinical course was complicated by persistent bilateral pneumothoraces, pleural effusion and Pseudomonas nosocomial infection. The man eventually recovered after 54 days in the ICU, and was transferred to a rehabilitation department.
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We investigated whether in vitro human endothelial and renal epithelial cells responded to torasemide or furosemide with enhanced secretion of the vasodilator prostaglandin prostacyclin (PGI2). We also investigated the effects of loop diuretics on plasma concentrations of PGI2 and its physiological antagonist thromboxane after 25 min of administration of drugs in 44 patients with congestive heart failure (CHF) and 44 healthy volunteers.
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Removal of external Ca2+ facilitated endogenous taurine release in cultured rat astrocytes. The stimulated release was not affected by furosemide, sucrose, tetrodotoxin and 3,4-dichlorobenzamil, but partially inhibited by nifedipine. Omission of external Na+ increased basal taurine release, and the effects of Na+ removal and Ca2+ depletion on the release were additive. The Na(+)-free condition did not affect Ca2+ paradox-induced cell death in astrocytes. These findings suggest that Ca2+ depletion facilitates taurine release in a mechanism independent of volume and the Na+ gradient and that the release is not involved in Ca2+ paradox-induced delayed cell toxicity in astrocytes.
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Acute toxicity study showed no fatality even with the highest dose and the diuretic study revealed significant diuretic activity (p < 0.05) in the dose of 3200 mg/kg.
To estimate the reproducibility of BOLD MRI measurements in the evaluation of intrarenal oxygenation levels.
To study the potential beneficial role of furosemide in resolving renal failure after hemofiltration in mechanically ventilated critically ill patients.
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The first-pass effect of furosemide was investigated in rats. Furosemide intravenous solution (20 mg kg(-1) Lasix), was administered via the jugular vein and the portal vein, orally, and instilled directly into the duodenum of rats. The first-pass effects of furosemide by lung, heart, and liver seemed to be negligible in rats. The absolute bioavailability of furosemide was 28.9 and 48.3% after oral and intraduodenal administration, respectively. Based on the gastrointestinal (GI) recovery study, 68.3 and 69.5% of furosemide were found to have disappeared mainly due to absorption and/or metabolism from rat GI tract after oral and intraduodenal administration, respectively. The results indicate that gastrointestinal and intestinal first-pass effects of furosemide were approximately 40% (68.3-28.9%) and 20% (69.5-48.3%) of the dose, respectively.
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Constipation and diarrhoea are common complaints and often reported as adverse drug reactions. This study aimed at finding associations between drugs and constipation and diarrhoea in a general population.
We assessed the acute bronchodilator effect of nebulized furosemide when added to conventional therapy of acute emergency department (ED) asthma. Using a double-blind design, 42 patients with acute asthma were randomized to receive 2.5 mg nebulized salbutamol and either 40 mg of nebulized furosemide or saline solution. We recorded clinical variables (respiratory rate, heart rate, and pulsus paradoxus) and peak expiratory flow rates (PEFR) before and 15 and 30 min after therapy. We found no significant difference in PEFR between salbutamol/furosemide and salbutamol/saline-treated patients 15 and 30 min following inhalation. Other endpoints were equally unaffected. However, when we examined separately those patients whose exacerbations were of relative short duration (< 8 hr), PEFR improved significantly more in the furosemide-treated group. At 15 min, PEFR increased by 82 +/- 48% in the furosemide group compared to 35 +/- 40% in the control group (p = 0.03), an effect that was also evident at 30 min when PEFR had increased by 113 +/- 49% in the furosemide group versus 61 +/- 35% in the control group (p = 0.014). Respiratory rate, heart rate, and pulsus paradoxus improved with no differences between the groups. The beneficial effect of furosemide was not evident in patients who reported more prolonged duration (> 8 hr) of asthmatic symptoms. The response to furosemide appeared to be unrelated to concomitant ED therapy with corticosteroids, to baseline pulmonary function, or to patient demographic variables. We conclude that furosemide may offer additive bronchodilator benefits in acute naturally occurring asthma of relative short duration.
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To determine whether the GABA-containing neurons in rat central nucleus of amygdala (CeA) can be activated by acute sodium deprivation.
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The effect of furosemide infusion was studied in 6 normal subjects and 6 patients with severe COPD and right ventricular failure during normoxemia and hypoxemia. In normal subjects, hypoxemia alone caused an insignificant (p less than 0.15) fall in plasma aldosterone concentrations (PAC). Intravenously administered furosemide resulted in significant (p less than 0.05) increases in PAC during both normoxemia and hypoxemia. After furosemide treatment mean arterial pressure (MAP) was significantly lower and arginine vasopressin (AVP) was significantly higher (p less than 0.05) with hypoxemia than with normoxemia. These changes in MAP and AVP were strongly correlated (r = -0.84). Urinary losses of water and sodium were similar after furosemide treatment with hypoxemia and normoxemia. In patients with right ventricular failure, neither changes in oxygenation nor furosemide infusion affected the markedly elevated baseline PRA and PAC levels. Arginine vasopressin levels were significantly higher with hypoxemia than with normoxemia, but urinary losses of water and salt did not differ between the 2 study days. We conclude that hypoxemia does not affect the PAC increase or urinary volume and sodium response to furosemide.
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Pharmacokinetic interactions involving anti-infective drugs may be important in the intensive care unit (ICU). Although some interactions involve absorption or distribution, the most clinically relevant interactions during anti-infective treatment involve the elimination phase. Cytochrome P450 (CYP) 1A2, 2C9, 2C19, 2D6 and 3A4 are the major isoforms responsible for oxidative metabolism of drugs. Macrolides (especially troleandomycin and erythromycin versus CYP3A4), fluoroquinolones (especially enoxacin, ciprofloxacin and norfloxacin versus CYP1A2) and azole antifungals (especially fluconazole versus CYP2C9 and CYP2C19, and ketoconazole and itraconazole versus CYP3A4) are all inhibitors of CYP-mediated metabolism and may therefore be responsible for toxicity of other coadministered drugs by decreasing their clearance. On the other hand, rifampicin is a nonspecific inducer of CYP-mediated metabolism (especially of CYP2C9, CYP2C19 and CYP3A4) and may therefore cause therapeutic failure of other coadministered drugs by increasing their clearance. Drugs frequently used in the ICU that are at risk of clinically relevant pharrmacokinetic interactions with anti-infective agents include some benzodiazepines (especially midazolam and triazolam), immunosuppressive agents (cyclosporin, tacrolimus), antiasthmatic agents (theophylline), opioid analgesics (alfentanil), anticonvulsants (phenytoin, carbamazepine), calcium antagonists (verapamil, nifedipine, felodipine) and anticoagulants (warfarin). Some lipophilic anti-infective agents inhibit (clarithromycin, itraconazole) or induce (rifampicin) the transmembrane transporter P-glycoprotein, which promotes excretion from renal tubular and intestinal cells. This results in a decrease or increase, respectively, in the clearance of P-glycoprotein substrates at the renal level and an increase or decrease, respectively, of their oral bioavailability at the intestinal level. Hydrophilic anti-infective agents are often eliminated unchanged by renal glomerular filtration and tubular secretion, and are therefore involved in competition for excretion. Beta-lactams are known to compete with other drugs for renal tubular secretion mediated by the organic anion transport system, but this is frequently not of major concern, given their wide therapeutic index. However, there is a risk of nephrotoxicity and neurotoxicity with some cephalosporins and carbapenems. Therapeutic failure with these hydrophilic compounds may be due to haemodynamically active coadministered drugs, such as dopamine, dobutamine and furosemide, which increase their renal clearance by means of enhanced cardiac output and/or renal blood flow. Therefore, coadministration of some drugs should be avoided, or at least careful therapeutic drug monitoring should be performed when available. Monitoring may be especially helpful when there is some coexisting pathophysiological condition affecting drug disposition, for example malabsorption or marked instability of the systemic circulation or of renal or hepatic function.
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Inflammatory reaction can be prevented by administration of anti-inflammatory drugs such as piroxicam but the prevention of increased permeability is unclear after overdistension of the bladder.
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The concentration of triiodothyronine (T3) in human serum is extremely low and can be determined only by very sensitive methods. We developed a homogeneous enzyme immunoassay for T3 analysis in unextracted serum.
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Out of a series of pyridine-3-sulfonylureas with diuretic activity torasemide (1-isopropyl-3- ([4-(3-methyl-phenylamino)pyridine]-3-sulfonyl)urea) has been proved to be one of the most active derivatives. In the rat, urinary volume and electrolyte excretions increased linearily with the logarithm of the dose, thus resembling the profile of a high ceiling diuretic. Experiments by oral and intravenous routes indicated that torasemide was equally potent both by oral and parenteral administration. Compared to furosemide, torasemide was 9-40 times more potent on weight basis in the rat. For the same natriuretic effect, however, potassium losses with torasemide were significantly less than with furosemide. The diuretic effect of torasemide lasted longer compared to that of furosemide. In accordance with the pharmacodynamic characteristics plasma elimination half-life of torasemide was about 1.5 h in the rat and bioavailability was nearly complete. Torasemide was 98-99% bound to plasma proteins. No in vitro interaction was found with the cumarine derivative warfarin.
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We searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, Chinese Biomedical Disc, VIP and China National Knowledge Infrastructure (CNKI).Date of last search: 4 July 2012
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Past research has demonstrated that when an animal changes from a previously drug-naive to an opiate-dependent and withdrawn state, morphine's motivational effects are switched from a tegmental pedunculopontine nucleus (TPP)-dependent to a dopamine-dependent pathway. Interestingly, a corresponding change is observed in ventral tegmental area (VTA) GABAA receptors, which change from mediating hyperpolarization of VTA GABA neurons to mediating depolarization.
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Nedocromil sodium, frusemide bumetanide and reversed osmosis water (control), were introduced by iontophoresis into the forearm skin of 10 volunteers in each of two single-blind studies. In study 1, histamine (20 microL of 100 microM) or vehicle was injected into the area of iontophoresis 10 min later. In study 2, histamine or vehicle was injected 5 mm outside the area of iontophoresis so the flare developed over the area of iontophoresis. Itch was scored on a visual analogue scale every 20 s for 5 min, flare areas were assessed using scanning laser Doppler imaging up to 10 min and weal was assessed by planimetry at 10 min.
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In this case, uncharacteristic clinical and laboratory findings led to an unanticipated diagnosis for a 24-year-old woman admitted for new-onset heart failure with features suggesting cardiac tamponade. Concomitant diagnosis of progressive mixed connective tissue disease associated with severe hypothyroidism was made. Despite early recognition (based on clinical and pathologic features) and rapid management (with glucocorticoids, thyroxine, metoprolol, lisinopril, furosemide, and milrinone), she deteriorated and died within 4 weeks.
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Biochemical tests revealed a nephrotic syndrome with a protein-loss in urine of 13.6 g/24 hours and a serum-albumin of 1.2 g/dl. Serological tests showed positive response for antinuclear antibodies, anti-double-stranded-DNA antibodies and cardiolipin antibodies. Renal histology revealed a lupus-associated diffuse membranous nephropathy (WHO-type Vd).
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Gitelman's syndrome is a rare autosomal recessive, renal tubular disorder, characterized by chronic hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria, and normal blood pressure. Patients usually present at a later age with episodic mild muscle weakness. Unexplained hypokalemia arouses suspicion. The diuretic loading test with furosemide and thiazide and the use of Bartter's normogram provides a practical and simple tool in comparison to the complex and costly genetic analysis, to confirm the diagnosis. Here we report a case of Gitelman's syndrome to show the utility of these simple techniques to explain the pathophysiology of the disease, as well as to localize the site of the renal tubular defect, to confirm the diagnosis.