Background & aims: Mechanisms of antral hypomotility with smoking are unknown. Slow wave disruption, which may be prostaglandin dependent, inhibits gastric motility. This study tested if nicotine reproduces motor 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 were performed in 9 nonsmokers and 9 smokers during transdermal nicotine treatment (14 mg). Studies were repeated after administration of 150 mg indomethacin daily for 3 days to test prostaglandin requirements of nicotine responses.
Results: Antral migrating motor complex periodicity and fasting and fed motility indices, not different in the groups under control conditions, decreased similarly in nonsmokers and smokers with nicotine. Tachygastria (> 4.5 cycle/min) increased from 2% +/- 2% to 16% +/- 3% of recording time, and arrhythmias (frequency instability index) increased from 0.5 +/- 0.1 to 1.1 +/- 0.2 cycle/min with nicotine in nonsmokers (P < 0.05), which normalized with indomethacin. Electrogastrography results were unchanged in smokers.
Conclusions: Nicotine evokes antral hypomotility in nonsmokers and smokers but evokes prostaglandin-dependent gastric dysrhythmias only in nonsmokers. Smokes show desensitization to nicotine-stimulated dysrhythmias. Thus, slow wave disruption is not essential to inhibit motor activity. This provides a model for the motor and myoelectric effects of smoking.