Inhibition of gastric motor activity by 16, 16-dimethyl prostaglandin E2
- 1 December 1985
- journal article
- research article
- Published by Springer Science and Business Media LLC in Digestive Diseases and Sciences
- Vol. 30 (12), 1181-1188
- https://doi.org/10.1007/bf01314054
Abstract
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 μg/kg) by itself increased a tonus of the gastric wall but dosedependently lessened the number and the amplitude of contractions. In those rats treated with 16-dmPGE2 (3 μg/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.This publication has 12 references indexed in Scilit:
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