Relationship between the gastric myoelectric and mechanical activity in the genesis of ulcers in indomethacin-insulin-treated rats.

We have proposed that gastric contractile activity mechanically induces ulcers in the nonsteroid antiinflammatory drug (NSAID)-treated rat. This study examines first the relationship between number (dose) of peristaltic contractions applied to the mucosa and the ulcer score. Second, it examines the relative roles of: altered gastric myoelectrical activity (MEA) resulting from indomethacin (Indo) pretreatment, insulin-induced gastric peristalsis, and a combination of the two in the generation of mucosal lesions. Third, it examines the effect of exogenous prostaglandin on the Indo-altered MEA and relates it to ulcerogenesis. Indo pretreatment increased gastric tone and MEA. In such animals, the dose of peristaltic contractions applied to the gastric wall was related to the ulcer score in a dose-dependent manner. Exogenous prostaglandin (PG) reversed the MEA effect of Indo and reduced ulceration. It is postulated that an altered smooth muscle state secondary to inhibition of prostaglandin synthesis (PG-S) renders the mucosa vulnerable to injury by peristaltic action.