Inhibition of gastric motor activity by 16,16-dimethyl prostaglandin E2. A possible explanation of cytoprotection.

Effects of 16-dimethyl prostaglandin E2 (16-dmPGE2) and necrotizing agents on gastric motility and gastric mucosa were studied in conscious rats. Gastric motility was determined using a miniature balloon positioned in the glandular part of the stomach, which was connected to a pressure transducer and polygraph. Necrotizing agents, such as absolute ethanol, 0.6 N HCl, 0.2 N NaOH, or 4 M NaCl, were instilled into the stomach through a small fistula prepared in the forestomach. One milliliter of these agents produced streak lesions in the glandular part of the stomach within 1 hr, which were preceded by violent gastric contraction in every case. An intragastric administration of 16-dmPGE2 (0.3-3 micrograms/kg) by itself increased a tonus of the gastric wall but dose-dependently lessened the number and the amplitude of contractions. In those rats treated with 16-dmPGE2 (3 micrograms/kg), necrotizing agents failed to enhance the motility or to induce streak lesions. Pretreatment with 1 M NaCl as a mild irritant also inhibited gastric motility and lesion formation, but those actions were significantly antagonized by indomethacin (5 mg/kg). These results indicate that necrotizing agents induce a violent gastric contraction, followed by development of lesions in the stomach, and that the inhibition of gastric hypercontraction may be involved in a cytoprotective action of a prostaglandin against those induced gastric lesions in rats.