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Department of Pharmacology, Faculty of Medicine, The University of Hong Kong, Hong Kong, People's Republic of China
Epidemiological
studies have shown that cigarette smoking is associated with peptic
ulceration. This study aims to investigate the mechanisms by which
cigarette smoking delays ulcer healing in rats. Gastric ulcers were
induced by applying acetic acid to the luminal surfaces in rats.
Twenty-four hours later, rats were exposed to different concentrations
of cigarette smoke (0, 2, or 4%) for a 1-h period once daily for 3 or
6 days. Cigarette smoke exposure delayed ulcer healing and decreased
gastric blood flow and angiogenesis at the ulcer margin. These changes
were accompanied by a significant reduction of constitutive nitric oxide synthase (cNOS) activity but not
PGE2 production and vascular endothelial growth factor levels. Administration of
L-arginine (10 mg/kg iv)
completely reversed the adverse actions on ulcer healing, gastric blood
flow, and angiogenesis in the mucosa at the ulcer margin but partially
restored angiogenesis in granulation tissues. In conclusion, cigarette
smoke exposure delays ulcer healing through depression of gastric blood
flow and angiogenesis at the ulcer margin. Reduction of cNOS expression
and activity is suggested to be involved in these ulcerogenic processes.
gastric blood flow; angiogenesis; prostaglandin E2; L-arginine
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