lasix 80mg tab
Sarcoidosis is a systemic disease with multiorgan involvement. In children, renal impairment of sarcoidosis usually is caused by either hypercalcemia leading to nephrocalcinosis or interstitial nephritis with or without granulomata. We report the case of a 13-year-old boy presenting with severe arterial hypertension and acute renal failure caused by an isolated sarcoid granulomatous interstitial nephritis (GIN). Other known causes of GIN, eg, drug intake or fungal or mycobacterial infection, were excluded, and there was no evidence of extrarenal sarcoid involvement. Renal function improved initially with prednisone treatment. Blood pressure was controlled using ramipril, nifedipine, furosemide, dihydralazine, and metoprolol. Later, the patient showed signs of severe steroid toxicity and progressive renal failure. Monthly treatment with infliximab, a tumor necrosis factor-alpha antibody, was started, resulting in steady improvement in renal function and resolution of renal granulomata. In addition, antihypertensive medication could be reduced, and low-dose prednisone therapy was maintained. To our knowledge, this is the first report of successful treatment with infliximab of a patient with sarcoid GIN.
lasix oral medication
Horses were exercised on a high speed treadmill, using a maximum speed of 13 m/s. During each exercise, airway pressures, airflow, esophageal and pulmonary artery pressures, and blood gas partial pressures were measured.
Although diuretics have been clinically shown to reduce cardiovascular morbidity and mortality, the effects of diuretics on cardiac hypertrophy are poorly understood. In this study, we examined the molecular effects of diuretics on hypertensive cardiac hypertrophy. Spontaneously hypertensive rats (SHR) were given p.o. M17055 (a novel "high ceiling" diuretic) 1.25, 2.5 or 5 mg/kg/day, furosemide 50 mg/kg/day or trichlormethiazide 30 mg/kg/day for 5 weeks. After the treatment, cardiac myosin isoforms were analyzed by gel electrophoresis, and cardiac hypertrophy-related gene expressions were examined by Northern blot analysis. These three diuretics significantly reduced cardiac hypertrophy of SHR. M17055 and furosemide, but not trichlormethiazide, significantly increased the proportion of cardiac V3 myosin of SHR by enhancing the gene expression of beta-myosin heavy chain. On the other hand, trichlormethiazide, but not M17055 or furosemide, suppressed the increased cardiac gene expression of skeletal alpha-actin in SHR. Cardiac collagen type III expression of SHR was decreased only by treatment with M17055. Plasma thyroid hormone levels of SHR were slightly decreased by M17055 and by furosemide and were negatively correlated with cardiac V3 myosin contents. Thus the effects on the gene expression of cardiac contractile proteins and collagen are significantly different among these three types of diuretics, which suggests that these diuretics may have different cardiac actions independent of their diuretic and antihypertensive actions. The increased cardiac V3 myosin induced by M17055 and by furosemide may be partially due to the decreased plasma thyroid hormone.
CS remains a notable medical problem observed in the emergency and paediatric intensive care units in Lebanon. Immediate prognosis is related to: immediate recognition of the CS, nature of the cardiopathy and initial response to therapeutic procedures such as rapid improvement of respiratory status and rapid diuresis. Echocardiography is a reliable, quick and non-invasive procedure for initial diagnosis.
The medical records of 150 children who underwent pyeloplasty from 1986 to 1995 were reviewed. After excluding nonevaluable cases a total of 127 renal units remained for investigation. Preoperatively each renal unit was examined with a standardized (well-tempered) furosemide stimulated renal scan. Postoperatively 60 renal units were evaluated with standardized diuretic renal scans at 3 and 12 months, 33 renal units at 3 months only and 34 renal units at 12 months only. Surgical success was defined by half-time less than 20 minutes on a standardized diuretic renogram.
In human endothelial and renal epithelial cells, both loop diuretics induced an increase of 6-KetoPGF1alpha secretion that reached a peak after about 5 min and remained stable for 30 min of exposure to the drugs. The magnitude of the phenomenon was lesser in epithelial than in endothelial cells. Moreover, in both cell lines, there was a significantly higher secretion of 6-KetoPGF1alpha to torasemide than furosemide (P < 0.05). Concentrations of 6-KetoPGF1alpha at baseline were similar between the groups of CHF patients receiving the two different drugs. After 25 min of both drugs, 6-Keto-PGF1alpha significantly increased (P < 0.01), and this was significantly higher in patients treated with 10 mg of torasemide (P < 0.05 vs furosemide). Levels of PGI2 at baseline were lower in healthy controls than those reached by CHF patients and similar between groups. After 25 min of both drugs, PGI2 plasma levels were significantly increased (P < 0.01). Baseline values of TxB2 were significantly higher in CHF patients compared with controls (P < 0.01 vs respective groups). and, more importantly, furosemide but not torasemide increased TxB2 levels in patients and controls (P < 0.05 vs baseline).
lasix gtt dosage
The mitochondria-rich epithelial cells of the renal medullary thick ascending limb (mTAL) reabsorb nearly 25% of filtered sodium (Na(+)) and are a major source of cellular reactive oxygen species. Although we have shown that delivery of Na(+) to the mTAL of rats increases superoxide (O(2)(·-)) production in mTAL, little is known about H(2)O(2) production, given the lack of robust and selective fluorescent indicators for determining changes within the whole cell, specifically in the mitochondria. The present study determined the effect of increased tubular flow and Na(+) delivery to mTAL on the production of mitochondrial H(2)O(2) in mTAL. H(2)O(2) responses were determined in isolated, perfused mTAL of Sprague-Dawley rats using a novel mitochondrial selective fluorescent H(2)O(2) indicator, mitochondria peroxy yellow 1, and a novel, highly sensitive and stable cytosolic-localized H(2)O(2) indicator, peroxyfluor-6 acetoxymethyl ester. The results showed that mitochondrial H(2)O(2) and cellular fluorescent signals increased progressively over a period of 30 min following increased tubular perfusion (5-20 nl/min), reaching levels of statistical significance at ∼10-12 min. Responses were inhibited with rotenone or antimycin A (inhibitors of the electron-transport chain), polyethylene glycol-catalase and by reducing Na(+) transport with furosemide or ouabain. Inhibition of membrane NADPH-oxidase with apocynin had no effect on mitochondrial H(2)O(2) production. Cytoplasmic H(2)O(2) (peroxyfluor-6 acetoxymethyl ester) increased in parallel with mitochondrial H(2)O(2) (mitochondria peroxy yellow 1) and was partially attenuated (∼65%) by rotenone and completely inhibited by apocynin. The present data provide clear evidence that H(2)O(2) is produced in the mitochondria in response to increased flow and delivery of Na(+) to the mTAL, and that whole cell H(2)O(2) levels are triggered by the mitochondrial reactive oxygen species production. The mitochondrial production of H(2)O(2) may represent an important target for development of more effective antioxidant therapies.
lasix 20mg cost
In patients with decompensated heart failure, absorption of orally administered furosemide may be delayed, possibly leading to impaired pharmacodynamic effects. Sublingual administration may represent an alternative in such situations.
lasix max dose
The primary efficacy end point was a change in 24-hour net urine output (UOP) from before to after thiazide-type diuretic administration, and the study was designed to test for the noninferiority of metolazone. Safety end points included changes in renal function and electrolyte concentrations. The mean dose of IV loop diuretic therapy (in IV furosemide equivalents) at baseline (before thiazide-type diuretic administration) was higher in the chlorothiazide group (mean ± SD 318.9 ± 127.7 vs 268.4 ± 97.6 mg/day in the metolazone group, p=0.004), but net UOP was similar (mean ± SD 877.0 ± 1189.0 ml in the chlorothiazide group vs 710.6 ± 1145.9 ml in the metolazone group, p=0.344). Mean doses of chlorothiazide and metolazone were 491 ± 282 mg and 5.8 ± 3.5 mg, respectively. Following thiazide-type diuretic administration, net UOP improved to a similar degree (2274.6 ± 1443.0 ml vs 2030.2 ± 1725.0 ml in the chlorothiazide and metolazone groups, respectively, p=0.308). For the primary efficacy end point, metolazone met the threshold for noninferiority by producing a net UOP of 1319.6 ± 1517.4 ml versus 1397.6 ± 1370.7 ml for chlorothiazide (p=0.026 for noninferiority). No significant differences in renal function were observed between the groups. Although hypokalemia was more frequent in the chlorothiazide group (75% with chlorothiazide vs 60.7% with metolazone, p=0.045), no significant differences in the rates of severe hypokalemia or other electrolyte abnormalities were observed between the groups.
Early goal-directed diuresis therapy can improve the prognosis of critical ill patients.
lasix dosage forms
Male gender, prematurity and delivery by cesarean section were the major risk factors for TTN. Parenteral furosemide had no effect on the clinical course. Peak respiratory rate (RRpeak) at the first 36 h was significantly higher in group 2 (P > 0.000). The cut-off for RRpeak during the first 36 h (RRpeak36) was 90/min and RRpeak36 > 90/min caused a 7.04-fold risk of prolonged tachypnea. White blood cell count and hematocrit levels were lower whereas duration of hospitalization and antibiotic treatment were longer in group 2.
lasix 5 mg
The estimated prevalence of thiamine deficiency in stable HF patients was calculated to be <11.6%. There was no correlation between diuretic dose and thiamine levels (r = 0.02, P = 0.93) and there was no correlation found between left-ventricular ejection fraction (LVEF) and thiamine levels (r = 0.147, p = 0.44).
lasix pill identifier
Pharmocodynamic dose-effect investigation.
lasix 10 mg
After 4-week treatment with 300 mg irbesartan + 12.5 mg hydrochorothiazide + 5 mg amlodipine, 86 patients with resistant hypertension were randomized to the add-on 25 mg spironolactone (MRB group, n = 46) or 5 mg ramipril (RASB group, n = 40) groups for 12 weeks. Treatment intensity was increased at week 4, 8 or 10 if home blood pressure (BP) was equal to or above 135/85 mmHg, by sequentially adding 20-40 mg furosemide and 5 mg amiloride (MRB group), or 10 mg ramipril and 5-10 mg bisoprolol (RASB group). Transthoracic echography was performed at baseline and week 12.
lasix gtt dose
The preliminary results demonstrate increased subcutaneous fat (increased skin fold thickness), greater muscle bulk (increased mid-upper arm and thigh circumferences) together with a significant elevation in plasma albumin and the hematocrit, which reflect the anabolic state in patients treated with ACE inhibitor-digoxin-diuretic with congestive heart failure.
lasix 75 mg
Malnutrition is common in children with congenital heart disease, while thiamine deficiency (TD) is common in malnutrition, in critically ill children, and in adults with congestive heart failure treated with loop diuretics. Our goal was to determine whether children with congenital heart disease had TD and whether treatment with loop diuretics is related to TD in these patients.
lasix 3 mg
Ionic perturbations occur during cortical spreading depression (SD), a phenomenon implicated in migraine pathophysiology. We studied the effect of 0.2, 2 and 20 mg kg-1 i.v. (n=4) furosemide on cortical direct current (d.c.) potential, cerebrovascular laser Doppler flux (rCBF[LDF]), artery diameter and NO concentration in the parietal cortex of the anaesthetized cat during repetitive SD. In vehicle-treated animals (n=4), SD activity was sustained for 50+/-1.8 min. However, duration of SD activity was significantly reduced when compared to vehicle to 39+/-6.6 (n=4), 34+/-8.5 (n=4) and 27.3+/-11.3 min (n=4), at 0.2, 2 and 20 mg kg-1 i.v. furosemide respectively. It is hypothesized that the mechanism of inhibition of SD d.c. activity by furosemide may be through alterations in cortical ion buffering capacity or inhibition of cell swelling in neurones or glia. These mechanisms may represent potential novel drug targets in future migraine therapy.
lasix fluid pill
Long-term diuretic therapy in stable infants with oxygen-dependent bronchopulmonary dysplasia, after extubation, improves their pulmonary function and decreases their fractional inspired oxygen requirement, but does not decrease the number of days that they require supplemental oxygen. The improvement in pulmonary function associated with diuretic therapy is not maintained after treatment is discontinued.
lasix drug interactions
No adverse effects or modifications of the blood pressure were observed after captopril administration. The diuretic response was deeply worsened by angiotensin converting enzyme inhibition in each hydronephrotic kidney even when the basal study was only slightly abnormal (15-minute washout basal -27 +/- 16%, after captopril -9 +/- 13, p <0.005). After surgical correction the diuretic washout during angiotensin inhibition appeared normal in all patients (15-minute washout -56 +/- 14%). Separate renal function and parenchymal transit of MAG-3 were not modified by angiotensin converting enzyme inhibition, preoperatively or postoperatively.
lasix 70 mg
The contribution that alpha6 subunit-containing GABA(A) receptors make to inhibitory synaptic transmission to granule cells was investigated by making whole-cell patch clamp recordings from granule cells in adult rat cerebellar slices and applying furosemide, the specific alpha6 subunit-containing GABA(A) receptor antagonist. Endogenous, extracellular GABA continually activated GABA(A) receptors producing a tonic current. Since this current was markedly reduced by furosemide it was probably produced by alpha6 subunit-containing receptors. In contrast, furosemide had little effect on the amplitude or kinetics of fast spontaneous inhibitory postsynaptic currents (sIPSCs), although such sIPSCs were abolished by bicuculline and SR95331. However, the amplitude of evoked IPSCs with a very slow rise and decay were markedly reduced by furosemide. These IPSCs probably resulted from the spillover of GABA from neighbouring synapses activating high affinity alpha6 subunit-containing receptors. In the rest of the cells (40 out of 46), evoked IPSCs had rise and decay kinetics that lay in-between fast sIPSCs and slow 'spillover' IPSCs. Such IPSCs had variable kinetics and also exhibited considerable variation in the magnitude of furosemide block. Thus the GABA(A) receptors present at adult Golgi cell-granule cell synapses, at a developmental stage where receptor expression is complete, are highly heterogeneous.
lasix recommended dosage
A well-established method to create an animal model for profound deafness is cotreatment with an aminoglycoside antibiotic and a loop diuretic. Recent data indicated that reduction of the aminoglycoside dose might yield selective high-frequency hearing loss. Such a model is relevant for studies related to hybrid cochlear implant devices, for example, with respect to preservation of residual hearing.
lasix normal dose
The tubular secretion of diuretics in the proximal tubule has been shown to be critical for the action of drugs. To elucidate the molecular mechanisms for the tubular excretion of diuretics, we have elucidated the interactions of human organic anion transporters (hOATs) with diuretics using cells stably expressing hOATs. Diuretics tested were thiazides, including chlorothiazide, cyclothiazide, hydrochlorothiazide, and trichlormethiazide; loop diuretics, including bumetanide, ethacrynic acid, and furosemide; and carbonic anhydrase inhibitors, including acetazolamide and methazolamide. These diuretics inhibited organic anion uptake mediated by hOAT1, hOAT2, hOAT3, and hOAT4 in a competitive manner. hOAT1 exhibited the highest affinity interactions for thiazides, whereas hOAT3 did those for loop diuretics. hOAT1, hOAT3, and hOAT4 but not hOAT2, mediated the uptake of bumetanide. hOAT3 and hOAT4, but not hOAT1 mediated the efflux of bumetanide. hOAT1 and hOAT3, but not hOAT2 and hOAT4 mediated the uptake of furosemide. In conclusion, it was suggested that hOAT1 may play an important role in the basolateral uptake of thiazides, and hOAT3 in the uptake of loop diuretics. In addition, it was also suggested that bumetanide taken up by hOAT3 and/or hOAT1 is excreted into the urine by hOAT4.
GABA(A) receptors are heteropentamers that are heterogeneously distributed at different synapses in the central nervous system. Although the modulation of GABA(A) receptors received much attention in hippocampal pyramidal cells, information is scarce regarding the pharmacology of these receptors in inhibitory interneurons. We investigated the pharmacological properties of GABA(A)-mediated miniature inhibitory postsynaptic currents (mIPSCs) using whole-cell voltage clamp recordings in two morphologically identified types of hippocampal CA1 interneurons, horizontal and vertical cells of stratum oriens-alveus. The negative modulators zinc (200 microM) and furosemide (600 microM) significantly decreased the amplitude of mIPSCs. Benzodiazepine agonists also produced significant effects: 10 microM zolpidem increased the amplitude, rise time, and decay time constant (decay tau) of mIPSCs, whereas 10 microM flunitrazepam affected similarly the amplitude and decay tau, but not the rise time. The neurosteroid allopregnanolone (10 microM) prolonged the decay tau of mIPSCs. Since these modulators act on different GABA(A) receptor subunits, this pharmacological profile suggests that GABA(A) receptors at spontaneously active inhibitory synapses onto vertical and horizontal interneurons are heterogeneous and formed by co-assembly of different combinations of subunits (alpha(1-5)beta(1-3)gamma(1-3)). Furthermore, these synaptic GABA(A) receptors appear in large part pharmacologically similar to those of pyramidal cells.
lasix 40mg tablet
The major outward chloride transporter in neurons is the potassium chloride co-transporter 2 (KCC2), critical for maintaining an inhibitory reversal potential for GABA(A) receptor channels. In a recent study, we showed that Zn(2+) regulates GABA(A) reversal potentials in the hippocampus by enhancing the activity of KCC2 through an increase in its surface expression. Zn(2+) initiates this process by activating the Gq-coupled metabotropic Zn(2+) receptor/G protein-linked receptor 39 (mZnR/GPR39). Here, we first demonstrated that mZnR/GPR39 is functional in cortical neurons in culture, and then tested the hypothesis that the increase in KCC2 activity is mediated through a soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE)-dependent process. We established the presence of functional mZnR in rat cultured cortical neurons by loading cells with a Ca(2+) indicator and exposing cells to Zn(2+), which triggered consistent Ca(2+) responses that were blocked by the Gq antagonist YM-254890, but not by the metabotropic glutamate receptor antagonist (RS)-α-methyl-4-carboxyphenylglycine (MCPG). Importantly, Zn(2+) treatment under these conditions did not increase the intracellular concentrations of Zn(2+) itself. We then measured KCC2 activity by monitoring both the rate and relative amount of furosemide-sensitive NH(4)(+) influx through the co-transporter using an intracellular pH-sensitive fluorescent indicator. We observed that Zn(2+) pretreatment induced a Ca(2+)-dependent increase in KCC2 activity. The effects of Zn(2+) on KCC2 activity were also observed in wild-type mouse cortical neurons in culture, but not in neurons obtained from mZnR/GPR39(-/-) mice, suggesting that Zn(2+) acts through mZnR/GPR39 activation to upregulate KCC2 activity. We next transfected rat cortical neurons with a plasmid encoding botulinum toxin C1 (Botox C1), which cleaves the SNARE proteins syntaxin 1 and synaptosomal-associated protein 25 (SNAP-25). Basal KCC2 activity was similar in both transfected and non-transfected neurons. Non-transfected cells, or cells transfected with marker vector alone, showed a Zn(2+)-dependent increase in KCC2 activity. In contrast, KCC2 activity in neurons expressing Botox C1 was unchanged by Zn(2+). These results suggest that SNARE proteins are necessary for the increased activity of KCC2 after Zn(2+) stimulation of mZnR/GPR39.
300 mg lasix
Intravenous pamidronate and subcutaneous calcitonin.
lasix 80 mg
Dogs with MMVD were treated with enalapril and furosemide for at least 1 month prior to examination. All dogs underwent standard and contrast echocardiographic examinations at the beginning of the study (T0). At this time, MMVD dogs were randomly assigned to receive either pimobendan (0.4-0.6 mg/kg) or not. All dogs with MMVD were re-evaluated by standard and contrast echocardiography after 1 week (T1) and nPTT and nMP were measured.
Studies were performed to evaluate the contribution of the urea appearance rate to the elevated plasma urea concentration found during diuretic-induced sodium depletion. Negative sodium balance of -1162 + 29 microEq/100 g body wt was induced over a four day period by the administration of furosemide, 20 to 30 mg/kg/d i.p., to rats ingesting a sodium free diet. When compared with sodium replete controls, sodium depletion significantly increased the plasma urea concentration (65.0 +/- 3.1 vs. 26.4 +/- 1.1 mg/dl) through both an increase in the urea appearance rate (160 +/- 5.2 vs. 125 +/- 3.5 mg/day/100 g body wt), and a decrease in the urea clearance rate (1.99 +/- 0.14 vs. 3.16 +/- 0.12 ml/min/kg). The urea appearance rate increased on the first day of diuretic administration, remained elevated three days after stopping diuretics, rapidly returned to control levels after sodium repletion, and was significantly correlated with the magnitude of sodium deficit. Similar results were obtained when diuretic-induced sodium depletion was produced in adrenalectomized animals. After four days of sodium depletion the plasma concentration was increased for some amino acids but not for the plasma total amino acid, nitrogen concentration. The results indicate that sodium depletion increases the urea appearance rate through a mechanism that is independent of adrenal function. Thirty to sixty percent of the elevation in plasma urea concentration that occurs in the rat during diuretic-induced sodium depletion can be accounted for by an enhanced urea appearance rate.