Abstract
Background: Tobacco cigarette smoke attenuates injury-induced hyperemia, aggravates hypertonic saline-induced mucosal damage, inhibits ulcer margin hyperemia, and increases the size of acetic acid-induced ulcer in the rat stomach. The inhibitory effect of tobacco cigarette smoke on gastric prostaglandin metabolism may be the basis for these observations. We have tested the hypothesis that exogenous prostaglandin (misoprostol) treatment will reverse these effects. Methods: Rats with these two types of gastric injury were treated with tobacco cigarette smoke or breathed room air and were given intragastric misoprostol or vehicle. Gastric mucosal blood flow was measured by hydrogen gas clearance, and lesion score or ulcer size was measured by image analysis. Results: Tobacco cigarette smoke attenuated the hyperemia and significantly aggravated the mucosal lesions and increased ulcer size. Treatment with intragastric misoprostol preserved the hyperemia and significantly attenuated the exacerbation of mucosal damage or increase in ulcer size produced by tobacco cigarette smoke. Conclusion: These data are consistent with the hypothesis that the attenuation of injury-induced or ulcer margin hyperemia by tobacco cigarette smoke is mediated by the inhibition of endogenous prostaglandins.