Comparsion of Effect of PRP,PDE5 Inhibitor in Treatment of Erectile Dysfunction

Erectile dysfunction (ED) is defined as the inability to attain and/or maintain penile erection sufficient for satisfactory sexual performance.The prevalence of erectile dysfunction (ED) increases with age, from 5% in men aged 20-39 years to 70% in men aged >70 years.

PDE5Is inhibit the enzyme phosphodiesterase-5 (PDE-5) present in the smooth muscle cells of the vessels. By inhibiting this enzyme, these drugs prevent the degradation of cGMP by PDE-5. GMP can cause activation of protein kinase G, leading to relaxation of the vascular smooth muscle. Prevention of degradation of cGMP by PDE-5 leads to the accumulation of cGMP in the vascular smooth muscle, thereby leading to dilatation of the blood vessels through phosphorylation of different downstream effector molecules. Dilatation of the penile arteries leads to a more prolonged erection. In addition, PDE5Is improve endothelial function and reduce apoptosis of vascular smooth muscle cells in the corpus cavernosum.

PRP is autologous plasma that has a platelet concentration above the concentrations typically found in whole blood and is derived from the patient's own blood (autologous) through a process of centrifugation.PRP has 7 fundamental proteins: platelet derived growth factors (PDGF), transforming growth factor-β (TGF-β), vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), and adhesive proteins - fibrin, fibronectin and vitronectin.

PDGF is a glycoprotein, which emerges from degranulation of platelets at the site of injection. It activates cell membrane receptors on target cell which in turn develop high energy phosphate bonds, which activates the signal proteins to initiate specific activity of target cells. These specific activities include mitogenesis, angiogenesis.