الفهرس 
INTRODUCTION AND AIM OF THE WORKOnly 14 pages are availabe for public view
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Abstract
In the present work , an attempt has been made to investigate the role of NO in the pathophysiologic mechanisms of gastric experimental ulceration as well as to answer some of the unresolved questions related to the interaction of NOS and COX products on gastric mucosa treated with LPS and if there is ant contribution of prostaglandin in this concert. Our results confirm and extend previous reports that bacterial endotoxin, LPS, originating from E.coli is capable of inducing iNOS activity in rat gastric mucosa ( Brown et al., 1994) and that this is associated with the inhibition of gastric acid secretion ( Tsuji et al., 1992) and the prevention of acute lesions in the gastric mucosa ( Tepperman and Soper, 1994 and Barrachina et al., 1995).