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6 resultats
The investigation of putative agents, using an in vitro model, to prevent cavernosal smooth muscle dysfunction during low-flow priapism.
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OBJECTIVE
To investigate the effect of putative agents for preventing irreversible smooth muscle dysfunction, using an in vitro model of low-flow priapism (a condition conventionally managed using a combination of corporal blood aspiration and instillation of alpha-adrenergic agonists), as failure
The effect of an antifibrotic agent, pirfenidone, on penile erectile function in an experimental rat model of ischemic priapism.
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To date, no effective medical approach for the treatment of erectile dysfunction (ED) secondary to ischemic priapism (IP) has been described. The aim of this study was to evaluate the anti-inflammatory, antifibrotic, and antioxidant effects of pirfenidone (PFD) on cavernosal tissue in a rat model of
Experimental priapism is associated with increased oxidative stress and activation of protein degradation pathways in corporal tissue.
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Priapism is a debilitating disease for which there is at present no clinically accepted pharmacological intervention. It has been estimated that priapism lasting more than 24 h in patients is associated with a 44-90% rate of ED. In this investigation, we determined in two animal models of priapism
Duration of priapism is associated with increased corporal oxidative stress and antioxidant enzymes in a rat model.
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Ischaemic priapism is characterised by hypoxia, hypercapnia and acidosis with resultant corporal fibrosis. Studies reported decreased erectile recovery after treatment of priapism longer than 36 h. However, a recent study revealed that half of patients with 3 days of priapism achieved recovery after
The effects of oxytocin on penile tissues in experimental priapism model in rats.
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Hematologic, biochemical, and cardiopulmonary effects of L-arginine supplementation or phosphodiesterase 5 inhibition in patients with sickle cell disease who are on hydroxyurea therapy.
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OBJECTIVE
Fetal hemoglobin (HbF) induction involves NO-cGMP signaling pathways. L-arginine, an NO precursor, and the phosphodiesterase (PDE) 5 inhibitor sildenafil, which potentiates cGMP, were studied in adults with sickle cell disease (SCD) who were stably on HU.
METHODS
Twenty four courses of
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