Fatemeh Nabavizadeh - Department of Physiology, Tehran University of Medical Sciences, Tehran, Iran
Rohallah Moloudi - Department of Physiology, Tehran University of Medical Sciences, Tehran, Iran
Ahmad Reza Dehpour - Department of Physiology, Tehran University of Medical Sciences, Tehran, Iran
Hossein Nahrevanian - Pasteur Institute of Iran, Tehran, Iran
Kaveh Shahvaisi - Department of Physiology, Tehran University of Medical Sciences, Tehran, Iran
Ehsan Salimi - Tehran University of Medical Sciences, Tehran, Iran

Objective(s) The liver has major role in the organism homeostasis, interactions with other systems, synthesis and metabolism of bile production, drug detoxification and hormone inactivation. Cholestasis can be defined as an impairment of the bile flow which can lead to hepatocytes necrosis and finally cirrhosis. Some studies reported a gastric acid secretion reduction in cirrhotic subjects, while others reported normal production gastric acid secretion. Our aim was to evaluate the effects of cholestasis and cirrhosis on gastric acid and pepsin secretions and its possible mechanism in rat. Materials and Methods Male Wistar rats were randomly divided into five groups (n= ۸): control, cholestasis, sham cholestasis, cirrhosis and sham cirrhosis. Laparatomy was done under general anesthesia and then bile duct ligation (BDL) was performed. After ۲ and ۴ weeks in cholestasis and cirrhosis groups respectively, gastric content was collected by wash-out technique. Basal and stimulated acid and pepsin secretions were measured by using titration and the Anson method respectively in all groups. In order to measure stimulated acid and pepsin secretions, pentagastrin (۲۵ pg/kg, i.p.) was used. Nitric Oxide (NO) metabolites of gastric tissue were determined by Griess microassy method. Results Acid and pepsin secretions were significantly reduced in cholestatic and cirrhotic rats in comparison with control and sham groups (P< ۰.۰۱). NO metabolite of gastric tissue was significantly increased in cholestatic and cirrhotic rats (P< ۰.۰۱). Conclusion Reducing of gastric acid and pepsin output in cholestatic and cirrhotic rats may be due to increasing in NO content of gastric tissue.

cholestasis, Gastric acid, Liver Cirrhosis, Nitric oxide, Pepsin