Use and synthesis method:

Use: This product is for scientific research only, not for other clinical trials. Sildenafil is a highly selective inhibitor of phosphodiesterase 5(PDE5), which is highly expressed in the corpus cavernosa penis and underexpressed in other tissues, including platelets, blood vessels and visceral smooth muscle and skeletal muscle. Sildenafil selectively inhibits PDE5, enhances the nitric oxide (NO)-cGMP pathway, and increases cGMP level, which leads to relaxation of smooth muscle of the corpus cavernosa, so that patients with erectile dysfunction can produce a natural erectile response to sexual stimulation. Erectile response was generally enhanced with the increase of sildenafil dose and plasma concentration. Experiments showed that the effect lasted up to 4 hours, but the response was weaker than that at 2 hours. Sildenafil's response to myocardium: PDE5 is not present in normal or diseased cardiac conduction tissue, cardiomyocytes, endothelial cells, and lymphoid tissue, so Sildenafil (PDE5 inhibitor) has no positive inotropic effect and cannot directly affect myocardial systolic function. Effects of sildenafil on cardiac parameters: A single dose of 100mg of sildenafil was taken orally in normal male volunteers without clinically significant ECG changes. In eight patients with stable ischemic heart disease, 40mg of sildenafil was administered intravenously in four separate doses under Swan-Ganz catheter monitoring, and systolic and diastolic blood pressure decreased by 7% and 10%, respectively, at rest from baseline. Resting right atrial pressure, pulmonary artery pressure, pulmonary wedge pressure and cardiac output decreased by an average of 28%, 28%, 20% and 7%, respectively.

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