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1 adalafil is a novel long-acting inhibitor of phosphodiesterase-5.
3 S-LTP identified vardenafil and Bay-73-6691 (phosphodiesterase-5 and -9 inhibitors, respectively) as
8 te mitochondria and that sildenafil-mediated phosphodiesterase 5 inhibition ameliorates dystrophic pa
10 of signaling downstream of endogenous NO by phosphodiesterase-5 inhibition protects against high fat
11 preserved ejection fraction enrolled in the PhosphodiesteRasE-5 Inhibition to Improve CLinical Statu
14 h preserved ejection fraction (HFpEF) in the PhosphodiesteRasE-5 Inhibition to Improve Clinical Statu
17 , therapeutic interventions, such as in vivo phosphodiesterase 5-inhibition, which effectively abroga
20 ric oxide donor sodium nitroprusside and the phosphodiesterase 5 inhibitor sildenafil compared with h
21 This study investigated the effect of the phosphodiesterase 5 inhibitor sildenafil on the pulmonar
24 ho was receiving treatment with tadalafil, a phosphodiesterase 5 inhibitor, developed bilateral, conc
29 candidates for treatment with either an oral phosphodiesterase-5 inhibitor or an oral endothelin-rece
30 onically inhibiting cGMP hydrolysis with the phosphodiesterase-5 inhibitor sildenafil improves energy
31 this study was to assess the effects of the phosphodiesterase-5 inhibitor sildenafil, on I/R injury
32 ts with SCD, administration of sildenafil, a phosphodiesterase-5 inhibitor that potentiates NO-depend
35 designed to evaluate effects of tadalafil, a phosphodiesterase-5 inhibitor used for the treatment of
40 Endothelin receptor antagonists (ERA) and phosphodiesterase 5 inhibitors (PDE5I) are long-term the
44 Early studies showed beneficial effects of phosphodiesterase 5 inhibitors on cardiovascular functio
46 mation by statins, pulmonary hypertension by phosphodiesterase 5 inhibitors, muscle weakness by exerc
49 ered by cinaciguat, riociguat, and different phosphodiesterase-5 inhibitors and beneficial actions of
51 promising recent research in treatment with phosphodiesterase-5 inhibitors in single ventricle patie
52 imental and human heart failure suggest that phosphodiesterase-5 inhibitors may enhance cardiovascula
55 rate that the increase of cGMP levels by the phosphodiesterase-5 inhibitors sildenafil and vardenafil
56 erosclerotic ED and a suboptimal response to phosphodiesterase-5 inhibitors were enrolled in this pro
57 lin and its analogs, endothelin antagonists, phosphodiesterase-5 inhibitors, and now a soluble guanyl
58 f ABCG2, such as tyrosine kinase inhibitors, phosphodiesterase-5 inhibitors, and the fumitremorgin-ty
59 ed nitric oxide, sodium nitrite, L-arginine, phosphodiesterase-5 inhibitors, niacin, inhaled carbon m
60 ith prostanoids, endothelin-1 inhibitors and phosphodiesterase-5 inhibitors, or a combination of ther
61 ailable-ie, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, soluble guanylate cyclas
65 ight benefit cardiovascular diseases because phosphodiesterase-5 is also located elsewhere in the bod
66 ivation and inhibition of the cGMP-degrading phosphodiesterase-5, ischemic preconditioning, and postc
67 ilable for immunohistochemical assessment of phosphodiesterase-5 isoenzyme (PDE-5) and PDE-2 expressi
77 e aim of this work was to test whether acute phosphodiesterase 5 (PDE5) inhibition via sildenafil (SI
78 dystrophin, restoration of nNOS effects by a phosphodiesterase 5 (PDE5) inhibitor (sildenafil) improv
81 rse of nitrate interaction with tadalafil, a phosphodiesterase 5 (PDE5) inhibitor with a half-life (t
82 gated whether sildenafil citrate (Viagra), a phosphodiesterase 5 (PDE5) inhibitor, can be used to ame
85 udies determined whether clinically relevant phosphodiesterase 5 (PDE5) inhibitors interacted with cl
88 by the chronic inhibition of cGMP-selective phosphodiesterase 5 (PDE5) suppressed maladaptive cardia
93 oth muscle cells (PASMCs), and inhibition of phosphodiesterase-5 (PDE5) has been shown to suppress TR
94 of vardenafil, a potent and highly selective phosphodiesterase-5 (PDE5) inhibitor, on symptom-limited
103 peting with this nucleotide for catalysis by phosphodiesterase-5 (PDE5), but the characteristics of d
104 ach competitively inhibit cGMP hydrolysis by phosphodiesterase-5 (PDE5), thereby fostering cGMP accum
106 d by cGMP-dependent allosteric activation of phosphodiesterase 5, which shapes the amplitude and dura
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