ライフサイエンスコーパス: furosemide

1 tions, and is inhibited by the loop diuretic furosemide.

2 R2* was elevated at baseline, but fell after furosemide.

3 low levels of R2* that did not change after furosemide.

4 ained before and after the administration of furosemide.

5 all benefit of administering both saline and furosemide.

6 l body irradiation unless NaCl is lowered by furosemide.

7 status were obtained prior to administering furosemide.

8 el is decreased by injection of the diuretic furosemide.

9 nd isoproterenol responsiveness depressed by furosemide.

10 icted and were maintained on stable doses of furosemide.

11 was not further impaired by papillectomy or furosemide.

12 1 antagonist, and also by 100 microM luminal furosemide.

13 oncentrate and dilute urine, and response to furosemide.

14 of INDO, followed immediately by 1 mg/kg of furosemide.

15 enally metabolized loop diuretic rather than furosemide.

16 id to the mitochondria was also prevented by furosemide.

17 not predictive of urinary output response to furosemide.

18 accumulation in the cytosol was prevented by furosemide.

19 er albumin regimen increased the response to furosemide.

20 fter the acute administration of intravenous furosemide.

21 n in NaCl concentration and by bumetanide or furosemide.

22 athways were activated by the diuretic drug, furosemide.

23 vehicle (sterile isotonic saline) instead of furosemide.

24 ys, 12 patients received placebo, BG9719 and furosemide.

25 iving BG9719 and 374 +/- 231 after receiving furosemide.

26 soxazole would restore response to 120 mg of furosemide.

27 irect pathway) in response to the actions of furosemide.

28 a decreased (p < 0.005) 63 +/- 18 following furosemide.

29 ut doubled in 20 patients (67%) following IV furosemide.

30 se to desmopressin and an intact response to furosemide.

31 nyl, metoprolol, lorazepam, hydralazine, and furosemide.

32 in rats by treatment with the diuretic drug, furosemide.

33 l derivative of the arylsulfonamide compound furosemide.

34 magnetic resonance imaging before and after furosemide.

35 tenuation was lower in patients who received furosemide (-0.1 HU) compared with those who did not (6.

36 Infants received intravenous furosemide (1 mg/kg every 6 hours) or a standardized PD

37 Thirty-two Yorkshire pigs were randomized to furosemide (1 mg/kg intramuscularly daily, mean 16.1 +/-

38 a baseline clearance, 1 group (F+V) received furosemide (1 mg/kg per hour) plus saline for 90 minutes

39 which involves intravenous administration of furosemide (1.0 or 1.5 mg/kg), can predict the developme

40 P < 0.02) and correspondingly lower tmax for furosemide (1.8 +/- 0.3 vs 4.2 +/- 1.2 hours, P = 0.006)

41 GABA-activated currents were insensitive to furosemide (10-1000 microM) in all NTS neurons tested.

42 in weight (-2.19 vs. -1.58 kg), intravenous furosemide (125 vs. 107 mg), discontinuation of the infu

43 20% mannitol (2.5 g/kg bolus every 6 hrs) or furosemide (2.5 mg/kg bolus every 6 hrs).

44 four treatments intravenously: (1) 40 mg of furosemide, (2) 25 g of albumin, (3) 40 mg of furosemide

45 eriment 1, animals treated with the diuretic furosemide (20 mg/kg) when denied access to saline exhib

46 Furosemide 200 mg/kg had no effect in 4/4 rats made acut

47 ague-Dawley rats received vehicle (group 1), furosemide (22 mg/100 g body wt per d) (group 2), or fur

48 seen less commonly in patients who received furosemide (27 of 111, 24%) than in those who did not re

49 n drinking water), four weeks of ALDO/salt + furosemide (40 mg/kg in prepared food), and four weeks o

50 experiments, rats were injected with either furosemide (5 mg) or vehicle solution (sterile isotonic

51 Baseline and furosemide (99m)Tc-MAG3 imaging examinations in 50 patie

52 mitochondria, an event that was inhibited by furosemide, a chloride channel inhibitor.

53 Furosemide, a loop diuretic, is commonly used in patient

54 ained before and after the administration of furosemide, a masked expert determined whether each kidn

55 addition, sIPSC frequency was attenuated by furosemide, a selective antagonist of alpha6 subunits.

56 Inhibition of TGF (by furosemide) abolished the l-NAME effect on the myogenic

57 We tested the hypothesis that furosemide accelerates the progression of left ventricul

58 re automatically extracted from baseline and furosemide acquisitions and forwarded to the expert syst

59 Furosemide activates the renin-angiotensin-aldosterone s

60 acute decompensated heart failure to receive furosemide administered intravenously by means of either

61 edullary hyperattenuation and the absence of furosemide administration (P = .002), younger age (P < .

62 yltriglycine ((99m)Tc-MAG3) scan followed by furosemide administration and a separate 20-min acquisit

63 In this experiment, furosemide administration increased the number of Fos-po

64 Furosemide administration prior to unenhanced CT is asso

65 or day of discharge if earlier, intravenous furosemide administration tended to be lower in the KW-3

66 nd the half-life of renal signal decay after furosemide administration was derived and compared with

67 in treatment between arms was predominantly furosemide administration, which was not associated with

68 odium excretion was 104 +/- 78 mEq following furosemide administration.

69 volunteers before and after water loading or furosemide administration.

70 However, in mice treated acutely with furosemide, administration of PDSinh-C01 produced a 30%

71 eritance with some cloned progeny exhibiting furosemide affinities outside the range of parental valu

72 ing of the 3D7A clone also exhibited altered furosemide affinities, implicating changes in one or mor

73 intravenous furosemide (n = 26), or 10 mg of furosemide alone (n = 26).

74 creted: 49 +/- 15 mg versus 54 +/- 12 mg for furosemide alone and furosemide plus sulfisoxazole, resp

75 Furosemide alone caused a decline in GFR.

76 Although administration of furosemide alone caused a large diuresis, addition of BG

77 Sodium excretion (mean +/- SD) from furosemide alone was 239 +/- 90 versus 240 +/- 115 mEq/8

78 ography may be supplemented with intravenous furosemide alone.

79 .01), a reduced pharmacodynamics response to furosemide also became important when creatinine clearan

80 Wild-type mice treated with furosemide, an inhibitor of NaK2Cl cotransporters, have

81 In the presence of furosemide, an inhibitor of the Na,K,Cl-cotransporter, N

82 for warfarin, 83.3% for ibuprofen, 70.0% for furosemide and 100% for sertraline in the top 10% of a l

83 f albumin premixed ex vivo, and (4) 40 mg of furosemide and 25 g of albumin infused simultaneously in

84 urosemide, (2) 25 g of albumin, (3) 40 mg of furosemide and 25 g of albumin premixed ex vivo, and (4)

85 ts of adenosine blockade in humans receiving furosemide and ACE inhibitors is unknown.

86 In the BNP-driven group, furosemide and acetazolamide were given more often and i

87 orter is dominated by loop diuretics such as furosemide and bumetanide, molecules used in clinical me

88 e Pfizer drug library, including ingliforib, furosemide and celecoxib, we successfully prepared stabl

89 1Fr activities were significantly reduced by furosemide and chlorothiazide treatment (P < 0.0001).

90 Furosemide and chlorthiazide are protective for unprovok

91 did not exhibit the natriuretic response to furosemide and exhibited a severely blunted response to

92 accompanies aldosteronism is aggravated with furosemide and is attenuated by spironolactone.

93 Four case studies on warfarin, ibuprofen, furosemide and sertraline implied that our method was ab

94 Natriuresis is effectively induced by both furosemide and the adenosine A1 antagonist BG9719 in pat

95 was reduced (p < 0.05) at week 4 ALDO/salt + furosemide and was accompanied by hypokalemia (<3.4 mmol

96 g 48 hr of sodium depletion with a diuretic (furosemide) and a sodium deficient diet, rats displayed

97 ffect of Na(+)-influx inhibitors ranolazine, furosemide, and amiloride was evaluated.

98 micals (bezafibrate, climbazole, diclofenac, furosemide, and hydrochlorothiazide), the measured persi

99 in DGCs were sensitive to allopregnanolone, furosemide, and loreclezole and insensitive to diazepam

100 e current and noise, were sensitive to Zn2+, furosemide, and loreclezole; they were insensitive to di

101 ined a greater urine output, and 3) received furosemide; and slower in those with high blood concentr

102 osterone levels were significantly higher in furosemide animals (43.0 +/- 11.8 ng/dl vs. 17.6 +/- 4.5

103 days in placebo versus 21.4 +/- 3.2 days for furosemide animals; p = 0.038, log-rank test).

104 chlear potential (EP) is reduced by means of furosemide applied chronically to one cochlea of a young

105 liable predictor of the urinary output after furosemide (area under the receiver-operating-characteri

106 However, furosemide-associated diuresis was reduced only in male,

107 Three patients were given furosemide at 30 min after the radiopharmaceutical and w

108 ons of 10 mCi (370 MBq) 99mTc-MAG3 and 40 mg furosemide (at zero time, or F0).

109 In addition, luminal furosemide attenuated the [NaCl]L-dependent changes in i

110 system was evaluated in 95 randomly selected furosemide-augmented patient studies (185 kidneys) obtai

111 Using furosemide (BCS class IV compound) as a model compound,

112 In addition, 20 patients received 20 mg of furosemide before late scans.

113 Albumin with furosemide benefits lung physiology in hypoproteinemic p

114 AVP neurons was reversed by bumetanide, and furosemide blocked AVP release, both in vivo and in hypo

115 ample, GABAA receptor antagonists, including furosemide, blocked the spontaneous current.

116 modest effects on serum pharmacokinetics of furosemide but had no effect on either the time course o

117 atory markers, and medullary R2* response to furosemide, but directly with GFR response to acetylchol

118 ed (p < 0.05) with ALDO/salt and ALDO/salt + furosemide, but not with spironolactone co-treatment.

119 SND formulation increased C(max) and AUC of furosemide by 36.6 and 43.2 fold respectively, relative

120 formulation enhanced the absorptive flux of furosemide by more than 3-fold.

121 KCC2 inhibition by furosemide caused a change in the intracellular Cl(-) co

122 that mimics the effects of the loop diuretic furosemide, ClC-Kb/K2 is assumed to have a critical role

123 and 970 +/- 137 microg/24 h, respectively); furosemide co-treatment further increased (p < 0.05) uri

124 creatinine clearance, hourly plasma/urinary furosemide concentrations, and hourly urinary output wer

125 d large effects on binding of bumetanide and furosemide, consistent with the hypothesis that loop diu

126 essive saline hydration and varying doses of furosemide continue to be the standard of care for emerg

127 metabolic improvements were not affected by furosemide cotreatment.

128 ne, but these changes were not attenuated by furosemide cotreatment.

129 of the cells with wortmannin, cycloheximide, furosemide, cyclosporin A, or decylubiquinone prevented

130 uivalent sodium and water excretion but only furosemide decreased GFR.

131 Furosemide-depleted rats that were allowed to drink 0.3

132 l medium reversibly inhibited transport, but furosemide did not.

133 ded mycophenolate, cyclosporine, prednisone, furosemide, diltiazem, aspirin, simvastatin, an angioten

134 A portion of the furosemide effect can be prevented by blockade of minera

135 Furthermore, post-STEP and furosemide effects interacted occlusively, both on E(GAB

136 Here, we identified stable differences in furosemide efficacy against PSAC activity induced by HB3

137 tics other than furosemide were converted to furosemide equivalent doses.

138 Loop diuretic dose (furosemide equivalent) was 80 (40, 140) mg with both nes

139 95% CI: 0.51 to 2.17), daily loop diuretic, furosemide equivalents >240 mg (HR: 1.49, 95% CI: 0.68 t

140 (interquartile range, 40-270) mg intravenous furosemide equivalents increased FELi by 12.6%+/-10.8% (

141 pilot: stable outpatients receiving >/=80 mg furosemide equivalents were studied before and after 3 d

142 s the net fluid output produced per 40 mg of furosemide equivalents, then dichotomized into high vers

143 Furosemide exaggerates these losses, whereas its combina

144 rongly associated with the amount of urinary furosemide excreted and was the only reliable predictor

145 reover, the relationship between the urinary furosemide excretion rate and the sodium excretion rate

146 ry sodium excretion and relating the urinary furosemide excretion rate to the sodium excretion rate.

147 pharmaceutical was administered 15 min after furosemide (F-15), whereas, in the second cohort of 29 p

148 cv infusions, rats were sodium depleted with furosemide, followed by the angiotensin-converting enzym

149 We also tested chlorthiazide and furosemide for seizure protection in animal models of ep

150 erefore, the coadministration of albumin and furosemide for the treatment of cirrhosis, and likely ot

151 etermine whether infants randomized to PD vs furosemide for the treatment of oliguria have a higher i

152 at PVP K12 and SDS were able to increase the furosemide free fraction available for oral absorption.

153 Furosemide (frusemide), which blocks only GABA(A),(fast)

154 he renal diuretic and natriuretic actions of furosemide (Fs) and retards the activation of aldosteron

155 their binding competitors, ibuprofen (IBU), furosemide (FUR) and tryptophan (TRP) were studied in ur

156 AJ balloons received a combined treatment of furosemide (Furo; 10 mg (kg bw)(-1)) plus a low dose of

157 ter and sodium by injections of the diuretic furosemide (Furo; 10 mg/kg, bw) and given a low dose of

158 and to what extent, with sulfamethazine and furosemide, giving rise to possible allergic or hypersen

159 ences in mortality (3 patients [9.4%] in the furosemide group vs 1 patient [3.1%] in the PD group) or

160 The furosemide group was 3 times more likely to have 10% flu

161 No difference was found between the PD and furosemide groups in the incidence of negative fluid bal

162 ine output </=125 ml/h following intravenous furosemide >/=40 mg).

163 and were receiving a continuous infusion of furosemide (> or =6 mg/kg/day).

164 Tachycardic pigs given furosemide had significant acceleration of both contract

165 When BG9719 was added to furosemide, however, creatinine clearance remained at ba

166 Chronic treatment with either enalapril, furosemide, hydralazine, or losartan were all effective

167 oth pharmacokinetics and pharmacodynamics of furosemide in acute kidney injury, and was the only reli

168 predictor of the urinary output response to furosemide in acute kidney injury.

169 e determinants of urinary output response to furosemide in acute kidney injury; specifically, whether

170 in failed to enhance the diuretic effects of furosemide in cirrhotic patients with ascites.

171 beneficial cardiorenal actions when added to furosemide in experimental heart failure.

172 hat aminophylline is an effective adjunct to furosemide in increasing diuresis in critically ill chil

173 n and a significantly attenuated response to furosemide in isolated TALH segments.

174 The use of furosemide in the management of hypercalcemia should no

175 ver, a review of the evidence for the use of furosemide in the medical management of hypercalcemia yi

176 Cotreatment with the diuretic furosemide in wild-type mice attenuated rosiglitazone-in

177 In mice treated long term with furosemide, in which renal pendrin is upregulated, PDSin

178 used a large diuresis, addition of BG9719 to furosemide increased diuresis, which was significant at

179 nts such as aminophylline, ascorbic acid, or furosemide increased or decreased endogenous wound elect

180 In these same patients, furosemide increased urine output at the expense of decr

181 In the accompanying paper, furosemide-induced activation in the NTS and caudal thor

182 Furosemide-induced activation in the SFO, OVLT, SON and

183 It is possible that the furosemide-induced activation in the SON and PVN is not

184 The furosemide-induced increase in urinary PGE(2) excretion

185 eriments lend support to our hypothesis that furosemide-induced neuronal activation in the thoracic s

186 ately when the patient was upright and after furosemide-induced volume depletion.

187 by a lumen-negative potential in response to furosemide infusion is abolished.

188 Moreover, furosemide-inhibitable transepithelial voltage is increa

189 In the second experiment, furosemide injection was preceded by treatment with a hi

190 icacy of hypertonic saline was equivalent to furosemide (ipsilateral, 82.09 +/- 0.50%; contralateral,

191 CK1-/- mice and acutely in normal mice given furosemide is associated with lower NTE mRNA and protein

192 However, the widely used KCC2 inhibitor furosemide is nonselective with antiseizure efficacy in

193 s with normal nephrograms, administration of furosemide led to a 20% decrease in medullary R2* (P < 0

194 In the case of the organic anion, furosemide, loss of renal secretion in the knock-out res

195 Cl(-); in recordings with low pipette Cl(-), furosemide lowered intracellular Cl(-), whereas in recor

196 AG3 scintigraphy with zero time injection of furosemide (MAG3-F0) was observed to display focal paren

197 permeability, and high first-pass effect of furosemide may also have produced the effect that small

198 otensin II type 1 receptor ligand, preserved furosemide-mediated natriuresis and diuresis, while redu

199 n] mum(2)/msec, P = .0059; or 1.86 +/- 0.07 [furosemide] mum(2)/msec, P = .0094).

200 mL of normal saline and 10 mg of intravenous furosemide (n = 26), or 10 mg of furosemide alone (n = 2

201 C mRNA demonstrated no significant effect of furosemide (NCC/glyceraldehyde-3-phosphate dehydrogenase

202 BG9719 on 1 day and the same medication plus furosemide on a separate day.

203 ponse (defined as weight change per 40 mg of furosemide on day 4 after admission) and hemoconcentrati

204 dition, the effects of a therapeutic dose of furosemide on glomerular filtration rate (GFR) and renal

205 tensin elicited by subcutaneous injection of furosemide on neural activation of the CNS.

206 Furosemide only delayed full-length Bid depletion and tB

207 Metal chelation, diuresis with furosemide or chlorothiazide, and competitive metal bloc

208 iment, rats were sacrificed 1.75 h following furosemide or saline injection by transcardial perfusion

209 ig ears deafened systemically (kanamycin and furosemide) or locally (neomycin).

210 on cotransport blockers, such as SITS, DIDS, furosemide, or bumetanide, when simultaneously added wit

211 albumin every 8 hrs with continuous infusion furosemide, or dual placebo, targeted to diuresis, weigh

212 midodrine plus octreotide, and dopamine plus furosemide over placebo to reduce mortality, and no ORs

213 nation of DMPS with either chlorothiazide or furosemide (P < 0.0001).

214 city of the kidney to secrete anionic drugs (furosemide) paralleled by an approximate 80% decrease in

215 Acute papillectomy or furosemide perfusion was performed to interrupt distal t

216 Furosemide pharmacokinetics were similar for all treatme

217 nd hourly urinary output were used to assess furosemide pharmacokinetics/pharmacodynamics parameters.

218 Rats receiving furosemide plus Losartan or furosemide plus the higher C

219 ed with furosemide plus the high CAP dose or furosemide plus Losartan.

220 de (22 mg/100 g body wt per d) (group 2), or furosemide plus spironolactone (22 and 20 mg/100 g body

221 versus 54 +/- 12 mg for furosemide alone and furosemide plus sulfisoxazole, respectively.

222 d not elaborate Fos in animals injected with furosemide plus the high CAP dose or furosemide plus Los

223 Rats receiving furosemide plus Losartan or furosemide plus the higher CAP dose did not show increas

224 Rats receiving furosemide plus the low CAP dose showed more Fos-positiv

225 as the other (F+T) received the same dose of furosemide plus TRV120027 (0.3 and 1.5 microg/kg per min

226 inflammation and robust STK-R2* responses to furosemide (possibly reflecting avid tubular oxygen cons

227 Patients with furosemide presented with lower SUV and radioactivity co

228 amiloride-blocked, and amiloride-blocked and furosemide-pretreated), PGE(2) caused relatively small (

229 Furosemide prevented all of these events.

230 The chloride channel inhibitor furosemide prevented intracellular alkalinization, Bax t

231 111, 24%) than in those who did not receive furosemide prior to imaging (79 of 178, 44%, P = .001).

232 se, 178 patients did not receive intravenous furosemide prior to imaging and 111 did.

233 ompared between patients who did not receive furosemide prior to imaging and those who did by using t

234 The Na/K/2Cl transport blocker furosemide produced cell shrinkage in isotonic solution

235 Interestingly, physical mixture containing furosemide, PVP K12 and SDS produced a similar level of

236 ine output correlated with cortical ADC with furosemide (r = 0.7, P = .034) and with medullary lambda

237 s in recordings with elevated pipette Cl(-), furosemide raised intracellular Cl(-).

238 Amiloride or furosemide reduced BP in CD ET-1 KO mice on a normal or

239 given at 0, 24, and 48 h, with a fixed-dose furosemide regimen as background therapy.

240 the addition of tolvaptan to a standardized furosemide regimen did not improve the number of respond

241 : (1) Continuation of RSG (RSG-C), (2) RSG + furosemide (RSG+FRUS), (3) RSG + hydrochlorothiazide (RS

242 uded that with either staurosporine or TNF a furosemide-sensitive change in pH(i) is linked to Bax tr

243 d perfusion of cultured cells indicated that furosemide-sensitive Cl- fluxes were located on the baso

244 effect correlates with the existing level of furosemide-sensitive K+-Cl- transport activity in the po

245 The furosemide-sensitive Na(+)-K(+)-2Cl(-) cotransporter (NK

246 The furosemide-sensitive Na(+)-K(+)-2Cl(-)-cotransporter (NK

247 he Na-K-2Cl-cotransporter NKCC2, and greater furosemide-sensitive Na+ reabsorption in association wit

248 m SPAK/OSR1 Ste20-type kinases, regulate the furosemide-sensitive NKCC2 and the thiazide-sensitive NC

249 The furosemide-sensitive potassium-chloride cotransporter (K

250 allied to in situ immunogold-EM analysis and furosemide-sensitive tonic current estimates revealed th

251 Furosemide shortened the time to left ventricular dysfun

252 repared food), and four weeks of ALDO/salt + furosemide + spironolactone (200 mg/kg/day in divided do

253 In early AKI, urine output after a furosemide stress test (FST), which involves intravenous

254 chaelian kinetics for inhibition of PESAC by furosemide, suggesting a 1:1 stoichiometry for their int

255 In mice, both chlorthiazide and furosemide suppressed the occurrence of maximal electros

256 even with dosing as high as 1,500 mg/kg for furosemide; TD50 was 549 mg/kg.

257 lpha][1,4]benzodiazepine-3 -carboxylate) and furosemide than those recorded from control DGCs.

258 eteral widths were significantly higher with furosemide than with saline for the middle (P </= .04) a

259 For ibuprofen-clarithromycin-furosemide, the elimination profiles were similar irresp

260 Albumin and furosemide therapy improves fluid balance, oxygenation,

261 The addition of albumin to furosemide therapy in hypoproteinemic patients with acut

262 ts were depleted of sodium with the diuretic furosemide three times (3F), one time (2V1F) or sham dep

263 tice has changed from F-15 administration of furosemide to an F + 0 protocol.

264 Intravenous administration of furosemide to pigs subjected to 1 hour of ileal ischemia

265 Application of the KCC2 blocker, furosemide, to control neurons mimicked E(GABA) shifts e

266 % (to 3532 +/- 113 units), compared with the furosemide-treated group (P < 0.005).

267 To answer this question, CCD from furosemide-treated mice were perfused in vitro, and the

268 In the short-survival experiment, the furosemide-treated rats had more Fos-positive cell nucle

269 iuria, and proteinuria of the -/- adults and furosemide-treated wild-type mice were unresponsive to i

270 In contrast, furosemide treatment did not produce more Fos-positive c

271 RVR responses during furosemide treatment, assuming complete inhibition of TG

272 on of angiotensin II that is generated after furosemide treatment.

273 ey to the central nervous system (CNS) after furosemide treatment.

274 paraventricular nucleus (PVN) in response to furosemide treatment.

275 When added to furosemide, TRV120027, a novel beta-arrestin biased angi

276 Among them, bumetanide and furosemide, two blockers of Na(+)/K(+)/Cl(-) cotransport

277 t had no effect on either the time course of furosemide urinary excretion or overall amount excreted:

278 When BG9719 was given in addition to furosemide, urine volume additionally increased and ther

279 rum sodium was reduced (133.0 +/- 0.9 mmol/l furosemide vs. 135.7 +/- 0.8 mmol/l placebo; p < 0.05),

280 Forty mg of oral furosemide was administered to 13 RYGB recipients and 14

281 Furosemide was administered to examine the effect of inh

282 ower at 3 h after injection, especially when furosemide was applied.

283 Stimulation of renin by furosemide was not affected by mPGES1 deficiency.

284 CI = 0.31-0.90), and a protective effect for furosemide was suggested (OR = 0.44, CI = 0.1-1.9).

285 target of the loop diuretics bumetanide and furosemide, we asked about their effects on HNS function

286 Forty milligrams of furosemide were administered to adults, whereas 0.5 mg/k

287 Additionally, the pharmacokinetics of furosemide were assessed.

288 Loop diuretics other than furosemide were converted to furosemide equivalent doses

289 amide, dichlorphenamide, chlorthalidone, and furosemide were not effective in vivo.

290 Mean opacification scores achieved with furosemide were significantly higher than those achieved

291 Though sulfamethazine and furosemide were used in this study; this principle and m

292 ortant sulfonamide drugs, sulfamethazine and furosemide, were taken and their binding to their respec

293 Treatment with furosemide, which decreases inner-medullary NaCl, reduce

294 uria was still observed after treatment with furosemide, which disrupts calcium and magnesium absorpt

295 Bumetanide and furosemide, which inhibit Cl- influx through the Na(+)-K

296 nal interstitial ATP concentrations, whereas furosemide, which is known to block TGF responses, reduc

297 s were equally randomly allocated to receive furosemide with albumin or furosemide with placebo for 7

298 ocated to receive furosemide with albumin or furosemide with placebo for 72 hrs, titrated to fluid lo

299 r secretion, and enhance the inactivation of furosemide within the kidney by glucuronidization.

300 The goal was to determine if furosemide would accelerate the progression of left vent