English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

The effect of 16,16-dimethyl prostaglandin E2 (dmPGE2) on gastric surface epithelial cell (SEC) damage induced by vagal nerve stimulation (VS) in urethane-anesthetized rats was studied using scanning electron microscopy. VS (1.25-10 Hz, 0.2 mA, 2 msec, 10 min) resulted in a graded increase in the SEC damage, increased gastric contractions, increased gastric acid secretion, and a decrease in heart rate. Pretreatment with dmPGE2 (0.3-30 micrograms/kg, s.c.) significantly protected the SEC from VS-induced damage, inhibited the increase in gastric contractions and acid secretion, but had no influence on the decrease in heart rate. Atropine (1 mg/kg, s.c.) also protected the SEC from VS-induced damage and inhibited the alterations in response to VS. Timoprazole (30 mg/kg, s.c.) had no protective effects on SEC from VS-induced damage, no effect on increased gastric contractions and heart rate, but did inhibit the increase in gastric acid secretion, in response to VS. These results suggest that: VS-induced SEC damage was caused by increased gastric contractions and not by increased gastric acid secretion, and dmPGE2 protects against SEC damage by inhibiting gastric contractions.

Effects of 16,16-dimethyl prostaglandin E2 on surface epithelial cell damage in the rat stomach induced by vagal nerve stimulation.