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Prevention of ethanol and aspirin-induced gastric mucosal lesions by paracetamol and salicylate in rats: role of endogenous prostaglandins.
Paracetamol or sodium salicylate given intragastrically 30 minutes before the administration of absolute ethanol or acidified aspirin dose-dependently reduced the formation of mucosal lesions and Indomethacin, the prostaglandin synthesis inhibitor, suppressed this effect and inhibited the protective influence of paracetamols or sodium Salicylates on the production of gastric lesions.
Release of Cholecystokinin by Amino Acids
The highest activity for release of CCK was exhibited by tryptophan and phenylalanine, which were also shown to release small amounts of secretin, which was 80% of the maximal response to exogenous CCK.
Protective action of omeprazole, a benzimidazole derivative, on gastric mucosal damage by aspirin and ethanol in rats.
It is indicated that omeprazole is capable of protecting gastric mucosa against ASA- and ethanol-induced injury and that this protection is unrelated to gastric inhibition or the biosynthesis of mucosal PGs.
Role of prostaglandins in the formation of aspirin-induced gastric ulcers.
It is indicated that gastric mucosa is capable of generating PGE2 and PGI2 which may be responsible for its protection against chemical injury.
Gastric protection by meciadanol
Meciadanol's action represents true cytoprotection, which was previously attributed only to prostaglandins, and the dose range of meciadanol that protected against ulcerogens did not affect either gastric acid secretion or pepsin output.
Effect of calcitonin on gastric and pancreatic secretion and peptic ulcer formation in cats
In conscious cats with chronic gastric fistula and the diversion of bile and pancreatic juice to the jejunum, calcitonin (5 U/kg-hr) caused a marked inhibition of near maximal gastric acid response
Gastric cytoprotection by prostaglandins, ranitidine, and probanthine in rats. Role of endogenous prostaglandins.
The cytoprotection appears to be the property not only of PGs but also of conventional gastric antisecretory compounds such as H2-receptor antagonists or anticholinergics.
Inhibition of gastric secretion by fat and hypertonic glucose in the dog: role of gastric inhibitory peptide.
It is concluded that GIP is unlikely to mediate fat‐induced inhibition of gastric secretion, but it is still possible that it might be involved in the inhibition that occurs during intestinal perfusion with hypertonic glucose solutions.
Comparison of vasoactive intestinal peptide and secretin in stimulation of pancreatic secretion.
The results of the combined study on cats and dogs suggest the possibility that oleate releases VIP from the gut and that this peptide may play a physiological role in the stimulation of pancreatic secretion.
Cytoprotective and ulcer healing properties of prostaglandin E2, colloidal bismuth and sucralfate in rats.
The preliminary results of 7- to 14-day treatment with certain drugs indicate that sucralfate and De-Nol, at the dose which does not affect gastric acid secretion, accelerated the healing rate of both gastric and duodenal ulcers so that the observed ulcer healing effect could be attributed to their ulcers healing property.