NICOTINE EFFECTS ON PROSTAGLANDIN-DEPENDENT GASTRIC SLOW-WAVE RHYTHMICITY AND ANTRAL MOTILITY IN NONSMOKERS AND SMOKERS

Background & Aims: Mechanisms of antral hypomotility with smoking are unknown. Slow wave disruption, which may be prostaglandin dependent, i nhibits gastric motility. This study tested if nicotine reproduces mot or effects of smoking and assessed the role of slow wave disruption in inducing hypomotility and the prostaglandin dependence of dysrhythmic responses. Methods: Electrogastrography and antroduodenal manometry w ere performed in 9 nonsmokers and 9 smokers during transdermal nicotin e treatment (14 mg), Studies were repeated after administration of 150 mg indomethacin daily for 3 days to test prostaglandin requirements o f nicotine responses. Results: Antral migrating motor complex periodic ity and fasting and fed motility indices, not different in the groups under control conditions, decreased similarly in nonsmokers and smoker s with nicotine. Tachygastria (>4.5 cycle/min) increased from 2% +/- 2 % to 16% +/- 3% of recording time, and arrhythmias (frequency instabil ity index) increased from 0.5 +/- 0.1 to 1.1 +/- 0.2 cycle/min with ni cotine in nonsmokers (P < 0.05), which normalized with indomethacin. E lectrogastrography results were unchanged in smokers. Conclusions: Nic otine evokes antral hypomotility in nonsmokers and smokers but evokes prostaglandin-dependent gastric dysrhythmias only in nonsmokers, Smoke rs show desensitization to nicotine stimulated dysrhythmias, Thus, slo w wave disruption is not essential to inhibit motor activity. This pro vides a model for the motor and myoelectric effects of smoking.