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 in the general population and are reduced by sildenafil.

4 with the phosphodiesterase type 5 inhibitor sildenafil.

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

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

7 A and B, but this effect was counteracted by sildenafil.

8 creased PBF heterogeneity is reversible with sildenafil.

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

10 0 minutes after oral administration of 50 mg sildenafil.

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

12 ecessary to allow the antifibrotic effect of sildenafil.

13 n restored PKG activation and enhancement by sildenafil.

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

15 reduce enhanced killing in combination with sildenafil.

16 ing supine bicycle exercise before and after sildenafil.

17 The most potent PDE5 inhibitor was sildenafil.

18 g the pulmonary vasodilation by imatinib and sildenafil.

19 hodiesterase inhibitor and lead compound for sildenafil.

20 ngioma that responded to treatment with oral sildenafil.

21 rPDEC1 in an orientation opposite to that of sildenafil.

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

23 contribute to variability in the efficacy of sildenafil.

24 sensitive to adriamycin and not protected by sildenafil.

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

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

27 topical NTG ointment application instead of 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 Does were randomized to receive either sildenafil 10 mg/kg/d or placebo by subcutaneous injecti

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

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

36 mum) that was significantly increased in the sildenafil (28.4 mum), NTG (28.8 mum) and combined (35.8

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

38 5 degrees ; P<0.001) and strain (Deltasigma: sildenafil, -3.30 +/- 1.86 versus placebo, 1.22 +/- 1.84

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

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

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

42 +/- 14%) who received a single oral dose of sildenafil (40 or 80 mg).

43 red to those in the ischaemic (63.2 and 3%), sildenafil (41.7 and 28.1%) and NTG (39.3 and 30.4%) gro

44 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

45 nstriction was reversed by administration of sildenafil (50 mg) to create four unique experimental co

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 We found that, sildenafil, a phosphodiesterase 5 inhibitor, induced mit

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

53 Sildenafil, a phosphodiesterase type 5 inhibitor, potent

54 Sildenafil, a phosphodiesterase-5 (PDE5) inhibitor causi

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

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

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

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

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

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

61 Although antenatal sildenafil administration rescues vascular abnormalities

62 After sildenafil administration, regional PBV-CV decreased in

63 a volume expansion but to a lesser extent by sildenafil administration; however, neither intervention

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

65 Sildenafil alone induced an improvement in the mean term

66 Administration of sildenafil alone was associated with a substantial incre

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

68 osterone levels or an inadequate response to sildenafil alone.

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

70 Sildenafil also improves blood flow in patients with BMD

71 Sildenafil also induces the expression of PGC-1 family m

72 Sildenafil also moderately inhibited the transport of E(

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

74 Thus, sildenafil ameliorates podocyte injury and prevents prot

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

76 Sildenafil, an FDA-approved phosphodiesterase 5 inhibito

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

78 denafil citrate suggesting the presence of a sildenafil analogue.

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

80 135 women and randomly assigned 70 women to sildenafil and 65 women to placebo.

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

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

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

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

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

86 Sildenafil and nitroglycerin (NTG) are vasodilator agent

87 ur analyses suggest that the combined use of sildenafil and NTG is more efficacious than using only o

88 The combined group were given both sildenafil and NTG treatments.

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

90 Neratinib interacted with the PKG activator sildenafil and the HMG CoA reductase inhibitor atorvasta

91 t model for CDH, the combination of maternal sildenafil and TO has a complementary effect on vascular

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 Before sildenafil, cardiac index increased throughout exercise

108 Sildenafil caused a modest decrease in mean systemic art

109 After sildenafil, choroidal thickness increased by 6.0% to 9.0

110 profiles showed a sustained drug release of sildenafil citrate for over 24 h.

111 onsidered as a potential alternative of oral sildenafil citrate for treatment of PAH.

112 ce time in comparison to orally administered sildenafil citrate of the same dose.

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

114 ocular imaging following treatment with oral sildenafil citrate, a phosphodiesterase type 5 (PDE5) in

115 at 1 and 3 hours after a 100 mg oral dose of sildenafil citrate.

116 n-vivo results for the pulmonary delivery of sildenafil citrate.

117 carrier for sustained pulmonary delivery of sildenafil citrate.

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

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

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

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

122 est that vascular response of the choroid to sildenafil decreases with age, but is not affected by th

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

124 The induction of PRC by sildenafil depends upon cAMP and the transcription facto

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

126 Sildenafil did not decrease filling pressure at rest or

127 Cilostazol and sildenafil did not have negative pharmacokinetic interac

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

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

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

131 INTERPRETATION: Sildenafil did not prolong pregnancy or improve pregnanc

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

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

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

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

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

137 Sildenafil dose was optimized, and 140 participants were

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

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

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

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

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

143 CDH fetuses treated with sildenafil, either with or without TO, had a medial thic

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

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

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

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

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

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

150 The sildenafil group were administered oral sildenafil treat

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

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

153 05; peak exercise, P=0.02) were lower in the sildenafil group.

154 il (HA-SIL) and Plasma Volume Expansion with Sildenafil (HA-PVX-SIL).

155 tude (HA), Plasma Volume Expansion (HA-PVX), Sildenafil (HA-SIL) and Plasma Volume Expansion with Sil

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

157 Sildenafil had a vasodilatory action and increased level

158 Sildenafil had no effect on any of the outcome parameter

159 Sildenafil had no effect on pulmonary artery systolic pr

160 Sildenafil had no effect on this parameter, while CDH fe

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

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

163 Sildenafil improved the renal blood flow for the first 3

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

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

166 dministration of the pulmonary vasodilatator sildenafil in a double-blinded and placebo-controlled tr

167 al vascular density remained unchanged after sildenafil in all 3 groups (P = 0.281-0.587).

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

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

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

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

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

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

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

175 5A:E90K polymorphism blunted the efficacy of sildenafil in terms of QOL improvement.

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

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

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

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

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

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

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

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

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

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

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

187 Sildenafil-induced improvement of LV contraction was acc

188 n of pulmonary arteries and a severe loss of sildenafil-induced pulmonary arteries relaxation.

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

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

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

192 Sildenafil inhibits cGMP efflux by binding to ABCC5, and

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

194 We hypothesized that sildenafil inhibits TRPC6 expression in podocytes throug

195 Sildenafil is a potent and selective inhibitor of the ty

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

197 Sildenafil is associated with reduced device thrombosis

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

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

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

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

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

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

204 Sildenafil may be a good translational candidate for hum

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

206 Cilostazol and sildenafil may benefit tuberculosis patients by shorteni

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

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

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

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

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

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

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

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

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

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

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

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

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

220 Sildenafil or pioglitazone treatment prevented proteinur

221 2.1 +/- 0.5 g/mL) were randomized to receive sildenafil or placebo (100 mg/d).

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

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

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

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

226 roidal expansion at 1 hour and 3 hours after sildenafil (P = 0.001) regardless of AMD status (P = 0.6

227 = 0.007), inhaled nitric oxide (P = 0.045), sildenafil (P = 0.004), had a shorter duration of vasoac

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

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

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

231 Intratracheally administered sildenafil particles elicited more pulmonary specific an

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

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

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

235 Sildenafil plus testosterone was not superior to sildena

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

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

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

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

240 Evidence shows that sildenafil protects placental perfusion and fetal growth

241 Sildenafil protects the fetal heart and circulation dire

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

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

244 Sildenafil reduces TRPC6 expression and activity in nonr

245 Sildenafil rescued the effects on mitochondria by Akt3 d

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

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

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

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

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

251 d whether the phosphodiesterase-5 inhibitor, sildenafil (SIL), could attenuate aortic root remodeling

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

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

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

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

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

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

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

264 In this study, response to sildenafil therapy was evaluated in dogs with PH by comp

265 QOL score were significantly improved after sildenafil therapy, and the plasma cGMP concentration wa

266 plasma cGMP concentrations before and after sildenafil therapy.

267 After sildenafil, there were no statistically significant diff

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 Sildenafil treatment after onset of chronic hypoxia prev

272 Sildenafil treatment also improved uterine blood flow, d

273 for the percent reduction in QOL score with sildenafil treatment by plasma cGMP level and by the PDE

274 Unexpectedly, sildenafil treatment did not affect mitochondrial conten

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

276 Sildenafil treatment failed to exert antiremodeling prop

277 This study showed that sildenafil treatment improved PH in dogs, and the PDE5A:

278 The sildenafil group were administered oral sildenafil treatment in addition to the same interventio

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

280 Sildenafil treatment protects placental perfusion and fe

281 Sildenafil treatment significantly increased myocardial

282 re when compared to the wildtype group after sildenafil treatment.

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

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

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

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

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

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

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

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

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

298 phenhydramine hydrochloride, rufinamide, and sildenafil, without any human intervention.

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

300 We hypothesized that sildenafil would reduce filling pressure during exercise