Possible Involvement of Non-Steroidal Anti-Inflammatory Drugs in Vagal-Mediated Gastric Acid Secretion in Rats

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Abstract
Effects of several non-steroidal anti-inflammatory drugs (NSAID) such as aspirin (ASA), indomethacin (IM), flurbiprofen (FP), ibuprofen (IP), phenylbutazone (PBZ) and flufenamic acid (FA) were studied on the gastric ulceration and gastric acid secretion induced by restraint and water-immersion stress (RWIS) or various secretagogues in rats. These drugs significantly increased ulcer formation. I.m. (1, 3 and 10 mg/kg s.c.) reduced gastric mucosal prostaglandin (PG) content dose-dependently. There was a correlation between the decrease in the PG content of gastric tissue and associated ulceration. The gastric acid secretion induced by the peripheral secretagogues, methacholine, gastrin and histamine, was not significantly influenced by I.m. pretreatment. The gastric acid secretion induced by the vagal mediated secretagogues, insulin, 2-deoxy-D-glucose (2-D-G) and RWIS, was markedly increased by i.m. pretreatment. These effects were not observed in vagotomized rats. By intracerebroventricular (i.c.v.) injection of IM, no influence was observed on the gastric acid secretion and ulcer formation induced by 2-D-G or RWIS. Acidic NSAID apparently potentiate the gastric acid output induced by stimulation of vagus nerve activity, and prostaglandins (PG) may influence gastric acid output by regulating vagus nerve activity.

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