Background: There is a high prevalence of impotence in patients with cirrhosis and
portal hypertension (PHT). Sildenafil is the most prescribed oral therapeutic agent for
patients with erectile dysfunction. It potentiates the effects of nitric oxide (NO)
released in the corpus cavemosum after sexual stimulation. Sildenafil is a selective
inhibitor of cGMP-specific phosphodiesterase type 5 (PDE5) in the corpus
cavemosum. Objective: As (PDE5) is also present in the mesenteric artery and some
other vascular.beds, the present study.aimed at investigation of sildenafil effects on
portal venous pressure (PVP) and mesenteric artery blood flow (MBF) in an animal
model of portal hypertension. Setting: Bertha Faculty of Medicine, Department of
Pharmacology. Methods: Sixteen male rabbits of local strain were used in this study.
The animals were divided into two equal groups each includes eight animals. The first I
group was sham-operated while the second group was operated to induce PHT by
partial ligation of the portal vein (PLPV). Animals were kept for three weeks then the
PVP and the MBF were recorded before and over 10 minutes after i.v injection of
sildenafil 1.0mg/kg. Results: The results of the present study revealed that sildenafil
1.0 mg/kg i.v significantly increased PVP and MBF in both sham-operated and PHT
groups with a percentage increase, which is less, pronounced in the PHT group.
Although these results suggested a vascular hyporesponsiveness to sildenafil in PHT,
they may have important implications in patients with cirrhosis and PHT as sildenafil
may lead to sudden increase in PVP and rupture of esophageal varices. In conclusion, I
sildenafil may be a risk factor in cirrhotic patients and should not be used in PHT to
avoid sudden episodes of hemorrhagic esophageal varices. |
