ライフサイエンスコーパス: sildenafil

1 ketoprofen, naproxen, sulfamethoxazole, and sildenafil).

2 erval, 4.5-50; P<0.001 versus no LLH, not on sildenafil).

3 sensitive to adriamycin and not protected by sildenafil.

4 eceived an additional 6 months of open-label sildenafil.

5 ecessary to allow the antifibrotic effect of sildenafil.

6 n restored PKG activation and enhancement by sildenafil.

7 KG) signaling, which was further enhanced by sildenafil.

8 reduce enhanced killing in combination with sildenafil.

9 ing supine bicycle exercise before and after sildenafil.

10 The most potent PDE5 inhibitor was sildenafil.

11 g the pulmonary vasodilation by imatinib and sildenafil.

12 hodiesterase inhibitor and lead compound for sildenafil.

13 ngioma that responded to treatment with oral sildenafil.

14 no LLH not on sildenafil, and (4) no LLH on sildenafil.

15 rPDEC1 in an orientation opposite to that of sildenafil.

16 fil group); none of these were attributed to sildenafil.

17 re randomized to low-, medium-, or high-dose sildenafil.

18 AF-A domain with higher sensitivities toward sildenafil.

19 ate full-length recombinant PDE5 affinity to sildenafil.

20 ts receiving therapy with either bosentan or sildenafil.

21 in the general population and are reduced by sildenafil.

22 with the phosphodiesterase type 5 inhibitor sildenafil.

23 RV-PA coupling may be uniquely sensitive to sildenafil.

24 umption and VE/CO2 slope were unchanged with sildenafil.

25 creased PBF heterogeneity is reversible with sildenafil.

26 nd 1 hour after administration of 20 mg oral sildenafil.

27 0 minutes after oral administration of 50 mg sildenafil.

28 ived placebo (-0.20 [IQR, -0.70 to 1.00]) or sildenafil (-0.20 [IQR, -1.70 to 1.11]) were not signifi

29 were randomized to receive modified-release sildenafil 100 mg once daily for 3 days followed by modi

30 : group A received 10 ppm of iNO followed by sildenafil (100 mg) orally 30 minutes later, and group B

31 inutes later, and group B initially received sildenafil (100 mg) orally followed by 10 ppm of iNO 60

32 delivery interval between women assigned to sildenafil (17 days [IQR 7-24]) and women assigned to pl

33 Patients were categorized as (1) LLH not on sildenafil, (2) LLH on sildenafil, (3) no LLH not on sil

34 bjects were randomized to receive placebo or sildenafil (20 mg three times daily) for 6 weeks.

35 aily for 3 days followed by modified-release sildenafil 200 mg once daily for 25 days or placebo.

36 fraction </= 50%) were randomized to receive sildenafil (20mg 3x daily) or placebo for 6 months.

37 adverse events in the sildenafil arm (45% of sildenafil, 22% of placebo, P = .022).

38 t fetal growth restriction to receive either sildenafil 25 mg three times daily or placebo until 32 w

39 zed as (1) LLH not on sildenafil, (2) LLH on sildenafil, (3) no LLH not on sildenafil, and (4) no LLH

40 5 degrees ; P<0.001) and strain (Deltasigma: sildenafil, -3.30 +/- 1.86 versus placebo, 1.22 +/- 1.84

41 ared with placebo in LV torsion (Deltatheta: sildenafil, -3.89 +/- 3.11 degrees versus placebo, 2.13

42 ypoxia (14% O2 ) from day 1 and treated with sildenafil (4 mg kg(-1) day(-1) ) from day 13 of the 21-

43 n on echocardiography were randomly assigned sildenafil 40 mg thrice daily or matching placebo for 9

44 +/- 14%) who received a single oral dose of sildenafil (40 or 80 mg).

45 ved placebo (15.0 m [IQR, -26.0 to 45.0]) or sildenafil (5.0 m [IQR, -37.0 to 55.0]; P = .92) were al

46 onolactone (21 [68%]), octreotide (7 [21%]), sildenafil (6 [19%]), fenestration creation (15 [48%]),

47 =0.026) and up to 60 min in the 18-hr group (sildenafil, 67.4 [38.0-87.0] vs. control 36.2 [30.5-50.0

48 flow for the first 30 min in the 2-hr group (sildenafil, 81.8 [43.8-101.9] vs. control 40.2 [6.4-76.9

49 erent at 24 weeks between placebo (95.8) and sildenafil (94.2) (P = .85).

50 Addition of sildenafil, a phosphodiesterase 5 (PDE5) inhibitor, in t

51 n (YFP) mouse, we investigated the effect of Sildenafil, a phosphodiesterase type 5 (PDE5) inhibitor,

52 Sildenafil, a phosphodiesterase type 5 inhibitor, potent

53 e would be resolved following treatment with Sildenafil, a treatment which rescues fetal growth.

54 his risk was reduced in patients with LLH on sildenafil (adjusted hazard ratio, 1.7; 95% confidence i

55 In group B, sildenafil administration also resulted in a significant

56 ordingly, we investigated the association of sildenafil administration and thrombotic events in patie

57 The hypoxemia after sildenafil administration in group B improved after the

58 Stimulation of PKG by measures such as sildenafil administration is potentially a new therapeut

59 After sildenafil administration, regional PBV-CV decreased in

60 otassium channel, 5-hydroxydecanoate, before sildenafil administration.

61 ABCB1 and non-ABCG2 substrate drugs, nor did sildenafil affect the function of another ABC drug trans

62 orbital and facial lymphangioma responded to sildenafil after repeated sclerosing and drainage proced

63 Administration of sildenafil alone was associated with a substantial incre

64 eline, after administration of either iNO or sildenafil alone, and at 90 minutes from baseline.

65 osterone levels or an inadequate response to sildenafil alone.

66 sized that a phosphodiesterase-5A inhibitor (sildenafil) alone or in combination with BNP would incre

67 Sildenafil also improves blood flow in patients with BMD

68 Sildenafil also moderately inhibited the transport of E(

69 using the chick embryo and hypothesised that sildenafil also protects fetal cardiovascular function i

70 Thus, sildenafil ameliorates podocyte injury and prevents prot

71 These data indicate that Sildenafil amplifies nestin expressing neural stem cells

72 Sildenafil, an FDA-approved phosphodiesterase 5 inhibito

73 Sildenafil, an inhibitor of cGMP-specific phosphodiester

74 nified' database was developed to detect the sildenafil analogue in Eurycoma longifolia products.

75 denafil citrate suggesting the presence of a sildenafil analogue.

76 nversion factors of 1.58 for ambrisentan and sildenafil and 1.52 for bosentan and tadalafil.

77 135 women and randomly assigned 70 women to sildenafil and 65 women to placebo.

78 ion in podocytes and counteracted effects of sildenafil and 8-Br-cGMP.

79 Short-term cGMP-enhancing treatment with sildenafil and BNP improves left ventricular diastolic d

80 Titin phosphorylation increased with sildenafil and BNP, whereas titin-based cardiomyocyte st

81 ricular diastolic capacitance increased with sildenafil and further with BNP (51.4+/-16.9 to 53.7+/-1

82 Plasma cGMP increased with sildenafil and further with BNP (7.31+/-2.37 to 26.9+/-1

83 o examine the effects of coadministration of sildenafil and inhaled nitric oxide (iNO) in patients wi

84 Emerging evidence indicates that sildenafil and other phosphodiesterase type 5 inhibitors

85 levels by the phosphodiesterase-5 inhibitors sildenafil and vardenafil induces a parallel release of

86 The risk estimates were similar for sildenafil and vardenafil or tadalafil.

87 filled prescriptions for the PDE5 inhibitors sildenafil and vardenafil or tadalafil.

88 interactions between PDE-Is (cilostazol and sildenafil) and rifampin.

89 il, (2) LLH on sildenafil, (3) no LLH not on sildenafil, and (4) no LLH on sildenafil.

90 ation of 2.5 ng/mL for the ERAs, 5 ng/mL for sildenafil, and 10 ng/mL for tadalafil.

91 ] iloprost, 118 [18%] sitaxsentan, 204 [31%] sildenafil, and 233 [36%] subcutaneous treprostinil).

92 ip during caval occlusion at baseline, after sildenafil, and BNP infusion.

93 y VLS to bind to ABCC5 were more potent than sildenafil, and the two most potent showed K(i) of 50-10

94 Sildenafil appeared to increase hospitalization rates fo

95 Although low doses of sildenafil are likely safe in pediatric PAH, further stu

96 PDE5 inhibitors (eg, sildenafil) are licensed for PH, but a role for PDE2 in

97 s experiencing serious adverse events in the sildenafil arm (45% of sildenafil, 22% of placebo, P = .

98 After sildenafil, arterial CSA decreased in SS smokers but did

99 These reported cases demonstrate promise for sildenafil as a noninvasive therapy for pediatric lympha

100 ministered, as a substitute for oral form of sildenafil, at a reduced dose and longer dosing interval

101 To determine whether the PDE5-inhibitor sildenafil benefits human dystrophinopathy, we conducted

102 s study shows that inhaled PLGA particles of sildenafil can be administered, as a substitute for oral

103 emonstrate that high sensitivity of PDE5 for sildenafil can be obtained not only through cGMP-induced

104 Before sildenafil, cardiac index increased throughout exercise

105 Sildenafil caused a modest decrease in mean systemic art

106 We have investigated whether sildenafil citrate (Viagra), a phosphodiesterase 5 (PDE5

107 Sildenafil citrate has been shown to induce myocardial p

108 We conclude that sildenafil citrate pretreatment augments myocardial func

109 lose match to the spectra of drug containing sildenafil citrate suggesting the presence of a sildenaf

110 a >/=10% increase in LVESV after 6 months of sildenafil compared to 13% (1 of 8) of subjects receivin

111 Phosphodiesterase-5 inhibition with sildenafil compared with a placebo had no effect on the

112 usside and the phosphodiesterase 5 inhibitor sildenafil compared with homozygous risk allele carriers

113 contractility was reduced by 11% to 16% with sildenafil compared with placebo (DeltaPWR/EDV -52+/-70

114 We therefore sought to determine whether sildenafil could improve exercise capacity in SCD patien

115 pite an initial clinical study demonstrating sildenafil-dependent amelioration of pathological remode

116 l novel ABCC5 inhibitors, we have identified sildenafil derivates using structural and computational

117 In contrast, sildenafil did not alter the sensitivity of parental, AB

118 Sildenafil did not decrease filling pressure at rest or

119 Cilostazol and sildenafil did not have negative pharmacokinetic interac

120 fter 18-hr CI (P=0.0.26), and treatment with sildenafil did not improve renal function in the 2-hr (P

121 tients with RVD and impaired RV-PA coupling, sildenafil did not improve RV function, exercise capacit

122 een RV-PA coupling and treatment effect, and sildenafil did not improve TAPSE, peak oxygen consumptio

123 INTERPRETATION: Sildenafil did not prolong pregnancy or improve pregnanc

124 an oral, intravenous, or intratracheal plain sildenafil did, when administered at the same dose.

125 cts with HF and preserved ejection fraction, sildenafil displayed opposing effects on ventricular and

126 and increased nitric oxide bioavailability; Sildenafil does not protect against fetal growth restric

127 had an unexplained increased mortality, all sildenafil dose groups displayed favorable survival for

128 eated patients were randomized to 1 of the 3 sildenafil dose groups.

129 Sildenafil dose was optimized, and 140 participants were

130 peak oxygen consumption (PV(O(2))) for the 3 sildenafil doses combined versus placebo.

131 Percent change in PV(O(2)) for the 3 sildenafil doses combined was only marginally significan

132 ren randomized to higher compared with lower sildenafil doses had an unexplained increased mortality,

133 RELAX trial would clarify the mechanisms of sildenafil effects and identify metabolites associated w

134 ntrast, eNOS activation, cGMP synthesis, and sildenafil efficacy were not estrogen dependent in male

135 In females, sildenafil-elicited myocardial PKG activity required est

136 Cotreatment with sildenafil enhanced DOX-induced apoptosis in PC-3 and DU

137 11 HF+EOV subjects treated with 12 weeks of sildenafil, EOV cycle length and amplitude decreased pro

138 to further assess the efficacy and safety of sildenafil, especially with chronic treatment.

139 esterase-5 inhibition with administration of sildenafil for 24 weeks, compared with placebo, did not

140 recently issued a warning against the use of sildenafil for pediatric PAH between 1 and 17 years of a

141 volume index increased (P=0.001) within the sildenafil group but was unchanged in the placebo group.

142 crease in PV distensibility (P=0.015) in the sildenafil group only.

143 udy (six in the placebo group and two in the sildenafil group); none of these were attributed to sild

144 (P=0.006) and peak exercise (P=0.02) in the sildenafil group, and systemic vascular resistance index

145 05; peak exercise, P=0.02) were lower in the sildenafil group.

146 Patients with LLH not on sildenafil had a greater increase in mean platelet volum

147 Sildenafil had a vasodilatory action and increased level

148 Sildenafil had no effect on any of the outcome parameter

149 Sildenafil had no effect on pulmonary artery systolic pr

150 Estrogen and sildenafil had no impact on pressure-overloaded hearts f

151 Although sildenafil has been shown to improve exercise capacity i

152 Here, we report that sildenafil has differential effects on cell surface ABC

153 Our results indicate that sildenafil has differential inhibitory effects on ABC tr

154 In Fontan patients, sildenafil improved cardiac index during exercise with a

155 Sildenafil improved the renal blood flow for the first 3

156 osphocreatine and myoglobin, suggesting that sildenafil improves dystrophic pathology through other m

157 s by a phosphodiesterase 5 (PDE5) inhibitor (sildenafil) improves skeletal and cardiac muscle perform

158 e and the phosphodiesterase type 5 inhibitor sildenafil in carefully selected patients with secondary

159 in males, the efficacy of the PDE5 inhibitor sildenafil in female cardiac pathologies has not been de

160 termined that the heart-protective effect of sildenafil in female mice depends on the presence of est

161 stoperative coadministration of iNO and oral sildenafil in patients with out-of-proportion pulmonary

162 erial Hypertension (STARTS-1) study assessed sildenafil in pediatric patients with pulmonary arterial

163 RTS-2 extension study; patients who received sildenafil in STARTS-1 continued the same dose, whereas

164 ting to the absence of benefit observed with sildenafil in subjects with HF and preserved ejection fr

165 gamma (PPAR-gamma) is a downstream target of sildenafil in the cyclic guanosine monophosphate (cGMP)-

166 g, and may be used as an alternative to oral sildenafil in the treatment of PAH.

167 en replacement restored the effectiveness of sildenafil in these animals.

168 The double-blind, placebo-controlled Sildenafil in Treatment-Naive Children, Aged 1 to 17 Yea

169 ebo orally 3 times daily for 16 weeks in the Sildenafil in Treatment-Naive Children, Aged 1-17 Years,

170 elective phosphodiesterase type 5 inhibitor, sildenafil, in a model of diabetic cardiomyopathy.

171 f VASP by the phosphodiesterase-5 inhibitor, sildenafil, in db/db mice reduced hepatic steatosis and

172 etabolites changed in the group treated with sildenafil, including decreased amino acids (alanine and

173 Sildenafil increased cardiac index (P<0.0001) and stroke

174 The apparent affinity for sildenafil increased from the nanomolar range to the pic

175 rogate substrate (GFPdgn), PKG activation by sildenafil increased myocardial proteasome activities an

176 tment of the ischemic middle-aged mouse with Sildenafil increased nestin expressing neural stem cells

177 Sildenafil-induced improvement of LV contraction was acc

178 Kidneys were treated with 1.4 mg/kg sildenafil infused 10 min before and for 20 min after re

179 tients who remain symptomatic on bosentan or sildenafil, inhaled treprostinil improves exercise capac

180 BCB1-overexpressing cells, nontoxic doses of sildenafil inhibited resistance and increased the effect

181 Similarly, in ABCG2-overexpressing cells, sildenafil inhibited resistance to ABCG2 substrate antic

182 man platelet, higher sensitivity of PDE5 for sildenafil inhibition has been detected after blocking c

183 ivated PDE5 with "super-high" affinities for sildenafil inhibition may be responsible for therapeutic

184 a "super-high" sensitivity state of PDE5 for sildenafil inhibition.

185 Sildenafil inhibits cGMP efflux by binding to ABCC5, and

186 h mitochondrial inhibitors, nitric oxide, or sildenafil inhibits proliferation of K-Ras-positive non-

187 Overall, we found that sildenafil inhibits the transporter function of ABCB1 an

188 We hypothesized that sildenafil inhibits TRPC6 expression in podocytes throug

189 Sildenafil is a potent and selective inhibitor of the ty

190 Because sildenafil is approved for clinical use, our results sug

191 Sildenafil is associated with reduced device thrombosis

192 Sildenafil is currently being clinically tested for the

193 hat the phosphodiesterase 5 (PDE5) inhibitor sildenafil is protective against hypertrophy-induced car

194 However, this trial suggests that sildenafil is unlikely to improve cardiac function in ad

195 ugh currently approved for use in adult PAH, sildenafil is used extensively off-label for the treatme

196 A potential new treatment, Sildenafil, is able to normalize the aberrant metabolomi

197 oma and associated ocular pain improved with sildenafil, making enucleation unnecessary.

198 Therefore, sildenafil may be a good candidate for human translation

199 Sildenafil may be a good translational candidate for hum

200 Modified-release sildenafil may be a treatment option in this patient pop

201 These findings suggest that sildenafil may be an important agent for improving exerc

202 Cilostazol and sildenafil may benefit tuberculosis patients by shorteni

203 We investigated the use of sildenafil-mediated cardioprotection in a rat model of h

204 cGMP pathways regulate mitochondria and that sildenafil-mediated phosphodiesterase 5 inhibition ameli

205 ance and frequent monitoring, and persistent sildenafil monotherapy is likely insufficient with disea

206 Sixteen-week sildenafil monotherapy is well tolerated in pediatric pu

207 Sildenafil (n = 113) or placebo (n = 103) administered o

208 Sildenafil (n = 79) or a placebo (n = 81) administered o

209 Compared with placebo (n=25), sildenafil (n=23) decreased Ea (-0.29+/-0.28 mm Hg/mL ve

210 ontrolled clinical study showed no effect of sildenafil on blood flow, maximal work capacity, and hea

211 ated exercise hemodynamics and the effect of sildenafil on exercise hemodynamics in Fontan patients.

212 rting the idea that the protective effect of sildenafil on fetal growth reported in mammalian studies

213 enter randomized trial testing the impact of sildenafil on peak VO2 in stable outpatients with chroni

214 We isolated the direct effects of sildenafil on the fetus using the chick embryo and hypot

215 effects of the phosphodiesterase-5 inhibitor sildenafil, on I/R injury in a porcine model of donation

216 Following treatment with Sildenafil, only 5 of the 18 previously identified diffe

217 Sildenafil or pioglitazone treatment prevented proteinur

218 2.1 +/- 0.5 g/mL) were randomized to receive sildenafil or placebo (100 mg/d).

219 r assessment before and after treatment with sildenafil or placebo in a prospective ancillary study.

220 of treatment with the pulmonary vasodilator sildenafil or placebo led to a 24.6% increase in PV dist

221 re randomized to low-, medium-, or high-dose sildenafil or placebo orally 3 times daily for 16 weeks

222 omly assigned to low-, medium-, or high-dose sildenafil or placebo orally thrice daily; within-group

223 = 0.007), inhaled nitric oxide (P = 0.045), sildenafil (P = 0.004), had a shorter duration of vasoac

224 et volume in comparison to those with LLH on sildenafil (P<0.001).

225 9), whereas it increased significantly after sildenafil (P=0.019).

226 cGMP remained unchanged before sildenafil (P=0.9), whereas it increased significantly a

227 Intratracheally administered sildenafil particles elicited more pulmonary specific an

228 occurred in 16 placebo patients (16%) and 25 sildenafil patients (22%).

229 occurred in 78 placebo patients (76%) and 90 sildenafil patients (80%).

230 enafil plus testosterone was not superior to sildenafil plus placebo in improving erectile function i

231 Sildenafil plus testosterone was not superior to sildena

232 The phosphodiesterase-5 inhibitor, sildenafil, potentiates NO signaling to inhibit platelet

233 Sildenafil preconditioning but not postconditioning sign

234 After 3 months, sildenafil produced a significant improvement compared w

235 lactic-co-glycolic acid) (PLGA) particles of sildenafil prolong the release of the drug, produce pulm

236 oxic development, and that the mechanisms of sildenafil protection include reduced oxidative stress a

237 Evidence shows that sildenafil protects placental perfusion and fetal growth

238 Sildenafil protects the fetal heart and circulation dire

239 Our findings indicate that modified-release sildenafil reduced attack frequency in patients with RP

240 Compared with baseline, after 60 minutes, sildenafil reduced systemic (-12%; P<0.001) and pulmonar

241 ng, while the addition of the cilostazol and sildenafil reduced the time to clearance by 1 month.

242 Sildenafil reduces TRPC6 expression and activity in nonr

243 se when types 3 and 5 PDE-Is (cilostazol and sildenafil, respectively) and rolipram were added to the

244 s randomized to low-, medium-, and high-dose sildenafil, respectively; 87%, 89%, and 80% were known t

245 These results demonstrate that sildenafil restores peripheral perfusion and reduces cen

246 on or by the phosphodiesterase 5a inhibitor, sildenafil, reversed HF feeding effects on ECM remodelin

247 ates dystrophic pathology, we tested whether sildenafil's benefits result from decreased mitochondria

248 In this cohort, sildenafil significantly improved ventilatory efficiency

249 The administration of sildenafil significantly increased the levels (P=0.047,

250 Mechanistic investigations revealed that sildenafil stimulated ABCB1 ATPase activity and inhibite

251 After taking sildenafil, subjects had a significantly decreased respi

252 However, sildenafil substantially blocked the increase in collage

253 eating PAH patients with oral or intravenous sildenafil suffers from the limitations of short dosing

254 Inhibition of PDE5 by sildenafil suppressed ET-1-induced activation of calcine

255 nes including a key intermediate involved in sildenafil synthesis has also been demonstrated.

256 the quantification of ambrisentan, bosentan, sildenafil, tadalafil, and their main metabolites.

257 ks per week was greater for modified-release sildenafil than for placebo (-44.0% versus -18.1%, P = 0

258 des a potential mechanism for the effects of sildenafil that, through adverse effects on mitochondria

259 Treatment with sildenafil, the cGMP derivative 8-bromoguanosine 3',5'-c

260 gical limitation, which can be attenuated by sildenafil, the clinical significance of which warrants

261 o the higher number of subjects worsening on sildenafil, the data and safety monitoring board recomme

262 ry Hypertension and Sickle Cell Disease with Sildenafil Therapy (Walk-PHaSST) study.

263 ry Hypertension and Sickle Cell Disease With Sildenafil Therapy cohort (allele frequency, 0.65; odds

264 Despite extensive clinical experience with sildenafil therapy in children and approval by the Europ

265 myotomy had no effect in these patients, but sildenafil therapy increased their ability to drink.

266 After sildenafil, there were no statistically significant diff

267 In addition, administration of sildenafil to inhibit PDE5 attenuated TAC-induced myocar

268 However, whether beneficial effects of sildenafil transcend onto the fetal heart and circulatio

269 and fetal growth, but whether the effects of sildenafil transcend the placenta to affect the fetus is

270 In STARTS-2, sildenafil-treated patients continued STARTS-1 dosing; p

271 and from 30.5 to 18.7 after modified-release sildenafil treatment (P = 0.244).

272 Sildenafil treatment after onset of chronic hypoxia prev

273 Sildenafil treatment also improved uterine blood flow, d

274 Doppler echocardiography showed that sildenafil treatment ameliorated DOX-induced left ventri

275 Unexpectedly, sildenafil treatment did not affect mitochondrial conten

276 ng the chick embryo model, here we show that sildenafil treatment directly protects the fetal cardiov

277 Sildenafil treatment failed to exert antiremodeling prop

278 ved no improvement in exercise capacity with sildenafil treatment in subjects with HF and preserved e

279 Sildenafil treatment protects placental perfusion and fe

280 using echocardiography, we show that chronic sildenafil treatment reduces functional deficits in the

281 Sildenafil treatment significantly increased myocardial

282 is 16-week, double-blind, placebo-controlled sildenafil trial.

283 An increased risk of melanoma in sildenafil users was recently reported.

284 Thus, we prepared porous PLGA particles of sildenafil using a water-in-oil-in-water double emulsion

285 study was a multicenter, randomized trial of sildenafil versus placebo in heart failure with preserve

286 potent phosphodiesterase-5 (PDE-5) inhibitor sildenafil (Viagra) induces a powerful effect on reducti

287 hat the increase of GIE stiffness induced by sildenafil (Viagra) is dependent on STEVOR phosphorylati

288 ly, the phosphodiesterase 5 (PDE5) inhibitor sildenafil was found to possess submicromolar affinity f

289 dium and high doses versus placebo; low-dose sildenafil was ineffective.

290 rone could improve erectile function without sildenafil was not studied.

291 stimated 3-year survival rates from start of sildenafil were 94%, 93%, and 88% for patients randomize

292 in PASMCs, while these inhibitory effects of sildenafil were abolished by PKG inhibitor Rp-8Br-cGMPs.

293 The protective effects of sildenafil were abolished by the putative blocker of the

294 ological variables and therapeutic effect of sildenafil were examined relative to the severity of RVD

295 istration of the phosphodiesterase inhibitor sildenafil, which augments eNOS function.

296 nt of mdx(5cv) mice with the PDE5 inhibitor, sildenafil, which was one of the six drugs impacting the

297 uction in pulmonary vascular pressures after sildenafil with no adverse effect on exercise hemodynami

298 deling predicted the binding conformation of sildenafil within the large cavity of the transmembrane

299 We therefore hypothesized that sildenafil would improve blood flow, maximal work capaci

300 We hypothesized that sildenafil would reduce filling pressure during exercise