Data from animal studies suggest that NSAIDs-induced gastric damage may be due to increased gastric motility. Such a mechanism, however, has never been tested or demonstrated in man. We evaluated the effects of two frequently prescribed NSAIDs, indomethacin and diclofenac sodium, on postprandial gastric motor activity (a physiologically reproducible stimulus) in healthy volunteers to see whether these compounds increase gastric motility. Twenty-four healthy volunteers of both sexes, 21-35 years of age, underwent a basal gastric motility recording. Thereafter, they were randomized in three groups to receive either placebo, indomethacin (50 mg three times a day) or diclofenac sodium (50 mg three times a day) for a week. At the end of the week, they underwent an identical manometric study. Analysis of the motility tracings showed no difference in gastric antral motility index and in amplitude of gastric antral contractions after NSAIDs with respect to the basal study and to the placebo group. About 50% of subjects (two in the placebo group) complained of side effects. These were transient and mild, except in two subjects taking indomethacin, in whom endoscopy was necessary; one of these had a small prepyloric ulcer. It is concluded that in man NSAID-related gastric damage is unlikely to be due to increased gastric motility.