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Three patients with possible cochleosaccular hydrops without vertigo were studied. The basis of diagnosis was positive result of the furosemide-loading vestibular evoked myogenic potential test, no canal paresis in the caloric test, and recurrent cochlear symptoms or fluctuating low-tone hearing loss.
Establishment of appropriate animal models is an important step in exploring the mechanisms of drug-induced ototoxicity. In the present study, using guinea pigs we compared cochlear lesions induced by cisplatin administered in two regimens: consecutive application alone and in combination with furosemide. The effects of furosemide alone were also evaluated; it was found to cause temporary hearing loss and reversible damage to the stria vascularis. Consecutive application of cisplatin alone appeared to be disadvantageous because it resulted in progressive body weight loss and higher mortality compared to the combined regimen, which used a smaller cisplatin dose. The combined regimen resulted in comparable hearing loss and hair cell loss but a markedly lower mortality. However, their coadministration failed to cause similar damage to spiral ganglion neurons (SGN), as seen in animals that received cisplatin alone. This difference suggests that the combined regimen did not mimic the damage to cochlear neuronal innervation caused by the clinical application of cisplatin. The difference also suggests that the SGN lesion is not caused by cisplatin entering the cochlea via the stria vascularis.
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A 38-year-old female patient on peritoneal dialysis (PD) due to type 1 diabetic nephropathy with a well-preserved residual renal function did not respond well to the conventional antihypertensive therapy consisting of candesartan, furosemide, and bunazosin. Switching candesartan for a fixed combination formula of candesartan plus hydrochlorothiazide (HCTZ) while the rest of the other two agents remained unchanged led to the remarkable reduction in both systolic and diastolic blood pressure (BP) without significant changes in the cardiothoracic ratio (CTR), body weight (BW), and residual renal function. This case suggests that when used in combination, diuretics acting on different functional segment of the nephron hold greater potential for enhanced antihypertensive effect, especially in patients on PD whose residual renal function is well preserved. A small dose of HCTZ with an angiotensin II receptor blocker (ARB) may partially explain the therapeutic benefit of this combination therapy in terms of a reliable hypotensive effect, a better adherence, and fewer side effects.
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A total of 52 renal units were studied under a prospective pressure-flow study protocol. All patients had grade 3 or 4 hydronephrosis (Society of Fetal Urology classification) and patient age range was 0.2 to 12 years (median 1.1). The suspected sites of obstruction were the ureteropelvic and ureterovesical junctions in 42 and 10 renal units, respectively. With the patient under general anesthesia 22 gauge percutaneous nephrostomy needles were inserted. Pressure-flow studies with an external infusion and/or furosemide induced diuresis were then performed. As the renal pelvic pressure progressively increased during the course of the pressure-flow studies, the renal pelvic pressure at which contrast material was first seen to appear distal to the suspected site of obstruction was recorded as the ureteral opening pressure. Ureteral opening pressures were compared to the results of the pressure-flow studies.
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To review the evaluation and management of the neonate and infant with prenatally detected hydronephrosis caused by a presumed ureteropelvic junction obstruction.
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The sequestration of cellular K(+) has been shown elsewhere to elicit a broad spectrum of antiviral activity. The obligatory, coupled cotransports of Na(+), K(+) and Cl(-) (NKCC1) and of Na(+) and K(+) (NKATPase) effect net cellular K(+) influx. We examined the effects of specific inhibitors of these transports; a cardiac glycoside (Digoxin) and a loop diuretic (Furosemide) on virus replication in vitro. The replication of the DNA viruses, herpes simplex virus, varicella zoster virus, human cytomegalovirus and adenovirus was inhibited. There was normal replication of the RNA virus encephalomyocarditis virus. Antiviral activities of both drugs were influenced by extracellular K(+). Antiviral effects were most potent when Digoxin and Furosemide were used in combination. Targeting the host cell in this way is fundamentally different to other antiviral drug developments to date and we propose the descriptive term Ionic Contra Viral Therapy (ICVT) for the purpose of definition. We believe that specific inhibitors of coupled K(+) transports merit controlled clinical trial for a broad spectrum of DNA virus infections by local application.
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Double-outlet right atrium (DORA) is a type of atrioventricular septal defect that is described as an extreme leftward deviation of the lower portion of the interatrial septum, resulting in insertion into the atrial wall left and posterior to the mitral orifice. This rare anomaly, which has been reported in humans and only just recently in cats, was identified by transthoracic echocardiography in a 9 year-old cat that was presented for further evaluation of a tachyarrhythmia and cardiomegaly. This case report describes the diagnostic findings in this cat and summarizes the anatomy, classification and clinical consequences of this rare congenital heart defect.
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The stability and compatibility of ceftazidime have been examined in the context of its potential use in concentrated solutions for continuous infusion in patients suffering from severe nosocomial pneumonia and receiving other intravenous medications by the same route. Ceftazidime stability in 4 to 12% solutions was found satisfactory (<10% degradation) for 24 h if kept at a temperature of 25 degrees C (77 degrees F) maximum. Studies mimicking the simultaneous administration of ceftazidime and other drugs as done in clinics showed physical incompatibilities with vancomycin, nicardipine, midazolam, and propofol and a chemical incompatibility with N-acetylcystein. Concentrated solutions (50 mg/ml) of erythromycin or clarithromycin caused the appearance of a precipitate, whereas gentamicin, tobramycin, amikacin, isepamicin, fluconazole, ketamine, sufentanil, valproic acid, furosemide, uradipil, and a standard amino acid solution were physically and chemically compatible.
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Effects of repeated administration of KW-3902, a novel adenosine A1-receptor antagonist, on its pharmacological actions were studied with regards to: 1) in vivo adenosine A1-antagonism, 2) diuretic effects and 3) renal protective effects against glycerol-induced acute renal failure (ARF). After repeated oral administration of KW-3902 (0.1 mg/kg/day) for 24 days, neither enhancement of the sensitivity to 5'-N-ethylcarboxamidoadenosine (NECA) nor reduction of the inhibitory effect of KW-3902 on the NECA-induced bradycardic response were observed. After repeated oral administration of KW-3902 (0.01 and 0.1 mg/kg/day) for 20 days, the diuretic effects of KW-3902 did not change. Renal protective effects against glycerol-induced ARF were not reduced by repeated oral administration of KW-3902 (0.01 and 0.1 mg/kg/day) for 23 days. These results suggest that repeated oral administration of KW-3902 has no effect on its pharmacological actions. Additionally, changes in serum parameters, which occurred after repeated administration of furosemide or trichlormethiazide, were minimal after repeated oral administration of KW-3902 (0.001-1 mg/kg/day) for 27 days. From these results, KW-3902 proved to be a diuretic which has renal protective effects with less side effects.
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A total of 8 of the 31 drugs tested (acyclovir, ceftriaxone, cefazolin, clindamycin, furosemide, heparin, pantoprazole, and piperacillin-tazobactam) were found to be physically incompatible with caspofungin.
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Patients aged >60 years with nocturia at least two voids per night were screened for enrollment into the study. A 3-week dose-titration phase established the optimum desmopressin dose (0.1, 0.2, or 0.4 mg). After a 1-week "washout" period, patients who showed sufficient response during the dose-titration period were randomized to receive staggered furosemide and the optimal dose of desmopressin or placebo in a double-blind design for 3 weeks. Voiding diaries were assessed before and after the treatment.
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An outwardly directed H(+)-gradient (pH 5.5 in/7.5 out) increased 22Na uptake into these vesicles. H+ gradient-driven 22Na uptake was significantly reduced by voltage clamping with K+/valinomycin, but was significantly stimulated by creation of an inside-negative potential. Potential sensitive 22Na uptake was inhibited by Na+ channel inhibitors phenamil and benzamil. Electroneutral 22Na uptake was insensitive to phenamil and benzamil, but was inhibited by amiloride, 5-(N,N-dimethyl)amiloride, 5-(N,N-hexamethylene)amiloride, and 5-(N-ethyl-N-isopropyl)amiloride. Electroneutral 22Na uptake showed saturation kinetics with an apparent Michaelis constant for Na+ of 11.8 +/- 2.4 mmol/L and a maximal velocity of 2.5 +/- 0.6 nmol.mg protein-1 x 5 s-1. The mechanism of amiloride inhibition was noncompetitive with an inhibitor constant for amiloride of 325 mumol/L. Acetazolamide, furosemide, bumetanide, 4-acetamido-4'-isothiocyano-2,2'-disulfonic acid stibene, and 4,4'-di-isothiocyanatostilbene-2,2'-disulfonic acid (1 mmol/L each) failed to inhibit 22Na uptake. Li+ and NH4+ (but not Cs+, K+, or choline+) inhibited H(+)-gradient driven 22Na uptake.
During continuous treatment with diuretics, the kidney adapts to the initial Na loss by activating antinatriuretic mechanisms which serve to prevent further Na and volume losses. To study the renal sites of adaptations to constant diuretic treatment, bendroflumethiazide (4 mg daily), furosemide (8 mg daily) or vehicle (0.24 ml daily) was infused intraperitoneally to female Wistar rats by implanted osmotic minipumps. Half of the animals (groups vol.) were randomized to receive a balanced saline solution to drink in addition to water in order to replace Na, K and volume losses. On the 6th day of treatment, clearances of inulin, Na, and Li were determined during four consecutive 6 hr periods. Circadian changes in renal excretions occurred in all groups with highest excretions of Na, Li and water in the dark period (6 p.m. to 6 a.m.). Renal changes induced by continuous infusion of diuretics were most pronounced in the dark period and would probably not have been disclosed if the clearance experiments had been restricted to the daytime. The average 24-hour clearance for inulin (glomerular filtration rate) was not different among groups, except for a 20% decrease in the furosemide group. The 24-hour fractional Na excretion, being approximately 0.5% in the vehicle group, increased to approximately 0.8% in group (bendroflumethiazide+vol) and to approximately 2.8% in group (furosemide+vol) but was not different from the vehicle group in the diuretic groups without volume replacement.(ABSTRACT TRUNCATED AT 250 WORDS)
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1008 ureteral segments were checked. For the image quality, readers did not find any significant difference (3.8 ± 0.5 vs 3.6 ± 0.7, p value: 0.13) between MRU methods. The interobserver agreement was excellent with a κ correlation coefficient as high as 0.89 for T2w-MRU and 0.92 for CE-MRU, respectively. For the detection of the segments and considering the 9 rotations for the T2W MRU, there were no statistically significant differences between the two groups.
A 16-month-old child developed a brief generalised tonic-clonic fitting episode and vomiting at home, after accidental ingestion of traditional massage oil. As the patient presented with clinical features of salicylate toxicity, appropriate management was instituted. He was admitted to the intensive care unit for multiorgan support. The child was discharged well 1 week after the incident. Methyl-salicylate is a common component of massage oils which are used for topical treatment of joint and muscular pains. However, these massage oils may be toxic when taken orally. Early recognition of the salicylate toxicity is very important in producing a good patient outcome.
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Furosemide is a class IV biopharmaceutical classification system drug having poor water solubility and low bioavailability due to the hepatic first-pass metabolism and has a short half-life of 2 h. To overcome the above drawback, this study was carried to prepare and evaluate the pellets containing furosemide solid dispersion (SD) for oral administration prepared by extrusion/spheronization. SD of furosemide was prepared with Eudragit L-100 at a drug-to-polymer ratio of 1:2 by employing a solvent evaporation method and characterized. Further, microcrystalline cellulose pellets containing SD were consequently prepared using a lab scale extrusion/ spheronizer and evaluated for in vitro drug release studies. The influence of process parameters used during extrusion/spheronization on the pellet properties was also studied using 2-factor, 3-level central composite design in order to improve the product quality. Additionally, the desirability function approach was applied to acquire the preeminent compromise between the multiple responses. Pellets containing solid dispersion (PSD) were prepared using optimal parameter settings demonstrated 88.52 ± 0.69% of the drug was released in a sustained release manner till 12 h. In vitro drug release data were fitted to various release kinetics models to study the mechanism of drug release. Drug release from the PSD was found to follow zero-order and Higuchi's model. Both studied parameters had great influence on the responses. PSD showed augmentation in the drug release profile till 12 h. The final optimized formulation was obtained by encapsulating best SD formulation within the pellet core to release the drug in the most soluble form in stomach and a sustained fashion in intestine.
In a prospective controlled study the frequency of arrhythmias during the early phase of acute myocardial infarction (AMI) was evaluated in 73 consecutive patients randomly assigned to either high or low dose furosemide prophylaxis. The high dose group (HDG) received 120 mg and the low dose group (LDG) 20 mg furosemide i.v. during the initial 24 hours in hospital. Increased diuresis, haemoconcentration and augmented heart rates were found in the HDG. No electrolyte disorders separated the groups. Hypokalemia was seen in two HDG patients and in one LDG patient on admission, and in two and three patients respectively after 24 hours. Continuous ECG recordings at a paper speed of 10 mm s-1 were obtained from all patients. Two patients in the HDG had ventricular fibrillation, none in the LDG. The number of patients with various arrhythmias was not significantly different in the two groups. Supraventricular tachyarrhythmias were more common in the HDG, whereas ventricular tachycardia and ventricular extrasystoles were seen more often in the LDG. We conclude that heart rate and recurrence of tachyarrhythmias in AMI may be influenced by furosemide therapy, seemingly through mechanisms other than electrolyte imbalance.
Determinations of renal oxygenation by blood oxygenation level-dependent magnetic resonance imaging (BOLD-MRI) in chronic kidney disease (CKD) patients have given heterogeneous results, possibly due to the lack of a reproducible method to analyse BOLD-MRI. It therefore remains uncertain whether patients with CKD have a reduced renal tissue oxygenation. We developed a new method to analyse BOLD-MRI signals and applied it to CKD patients and controls.
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Combination of both furosemide and albuterol led to significant increase in peak flow rate but it did not significantly affect FEV1, FVC, FEF 25-75, respiratory rate, SaO2 or clinical scores as compared to other groups. There were no significant adverse effects from the three drugs used.
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The geometric mean urinary protein/creatinine ratio was lower with combined ramipril at 5 mg/day, valsartan at 80 mg/day and increased furosemide dosage compared to combined ramipril at 5 mg/day and valsartan at 80 mg/day, but also to combined ramipril at 10 mg/day and valsartan at 160 mg/day. These differences remained significant after adjustment for SBP, DBP or MAP and 24-hour natriuresis but not after adjustment on eGFR. Diuretic dosage uptitration did not increase the number of home systolic blood pressure measurements below 100 mmHg, but led to a statistically significant increase in the number of symptomatic hypotension episodes.
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The mice chronically treated with 30 mg/kg/day furosemide displayed a significant polyuria (2.1 ± 0.3 and 1.3 ± 0.2 mL/24 h, furosemide versus control respectively, P < 0.05). Furosemide treatment resulted in increased serum concentrations of Na(+) [158 ± 3 (treated) and 147 ± 1 mmol/L (control), P < 0.01], whereas serum K(+), Ca(2+) and Mg(2+) values were not significantly altered in mice treated with furosemide. Urinary excretion of Na(+), K(+), Ca(2+) and Mg(2+) was not affected by chronic furosemide treatment. The present study shows specific renal upregulation of TRPM6, NCC, TRPV5 and calbindin-D28K.