الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 152 |  |  |
| | | from | 152 | | |
Abstract
Portal hypertension (PHT) is a progressive,
inevitable consequence of cirrhosis of liver, which
accounts for most of the severe complications of
cirrhosis. Portal hypertension leads to the formation of
portosystemic collateral veins. (Faiz et al., 2013).
Gastroesophageal varices (GOVs) are a result
of portal hypertension which are usually present in
about 50% of cirrhotics at the time of diagnosis, have a
growth rate potential of 7% per year and a 1-year rate of
first variceal hemorrhage ranging from 5 to 15% with
approximately a 6-week mortality rate of 15–20% with
each episode (Garcia-Tsao and Bosch , 2010).
GVs may be seen in 18%-70% of the patients
with portal hypertension and are probable source of
bleeding in 10%-36% of patients with acute variceal
bleeding. Isolated GVs, without EVs, are seen in 5%-
12% of patients with PHT (De Franchis, 2010).
The majority of serotonin in the body (90%) is
synthesized by enterochromaffin cells of the
gastrointestinal (GI) tract, where it regulates intestinal
motility (Gershon, 2013).
Serotonin, at the level of hepatic sinusoids,
causes endothelial fenestrae contractions of liver
sinusoids through 5-HT1 receptors mediated by a Ca2+-
dependent process. Due to different pro-inflammatory
mediators releasing from the damaged liver, it comes to
platelet adherence to sinusoidal endothelium,
translocation into Disse‘s space and serotonin release.