1,721,037 research outputs found
Cimetidine inhibition of dimaprit-induced writhing in the rat.
No full textIntraperitoneal, but not intravenous administration of dimaprit (50-125 mg/kg) caused a dose-dependent writhing in the rat. This effect was blocked, again in a dose-dependent fashion, by cimetidine administered orally 1 h prior to dimaprit. Results obtained suggest that dimaprit induces a cimetidine-sensitive pain by acting at peripheral nociceptive terminals within the peritoneum. The specific (H2-receptor related) analgesic effect of cimetidine could explain its effectiveness in relieving epigastric pain of duodenal ulcer patients treated with the drug
Antioxidant activity of a nitro derivative of aspirin against ischemia reperfusion in hamster cheek pouch microcirculation
No full textThe effect of the new H2-receptor antagonist mifentidine on gastric secretion, gastric emptying and experimental gastric and duodenal ulcers in the rat: comparison with cimetidine and ranitidine.
No full textThe new H2-receptor antagonist mifentidine (DA 4577) was tested for its antisecretory and gastric motor effects in comparison with cimetidine and ranitidine. The Shay rat preparation (5 h) was used for studying gastric secretion; the gastric emptying of a liquid meal was chosen for studying gastric motility. All the three compounds inhibited acid secretion in a dose-dependent fashion. Calculated ED50s were 2.3, 12.2 and 92.8 mg X kg-1 for mifentidine, ranitidine and cimetidine, respectively. Therefore, in this animal model, mifentidine was about 40 times more potent than cimetidine and 5 times more potent than ranitidine. As far as gastric emptying is concerned, the effect of equiactive antisecretory doses (i.e. the respective ED50s calculated from the previously established dose-response curves) of all the three antagonists was completely different. Cimetidine delayed emptying rate, whereas ranitidine accelerated it and mifentidine was completely ineffective. However, at higher doses, also this compound affected emptying rate by reducing it dose-dependently. Gastric and duodenal ulcers were induced in the rat by dimaprit (100 mg X kg-1 intravenously) and cysteamine (250 mg X kg-1 subcutaneously), respectively. As far as gastric ulcer is concerned, the ED50s (the effective dose which protected 50% of the animals from lesions) were 0.23, 4.40 and 9.70 mg X kg-1 for mifentidine, ranitidine and cimetidine, respectively. As regards duodenal ulcer, the ED50 was 4.48 for mifentidine and 150.00 mg X kg-1 for ranitidine. In this animal model, the efficacy of cimetidine was very low. Therefore an ED50 could not be determined. In conclusion, results of the present investigation demonstrated that mifentidine is a potent antisecretory compound and an effective anti-ulcer agent in the rat
Oxygen free radicals interact with indomethacin to cause gastrointestinal injury.
No full textIn the present study it was shown that, unlikely MK447, a known oxygen free radical compound, PGE2 is much less effective against indomethacin-induced G.I. ulcers than against ethanol damage. It seems likely that factors other than PG deficiency (such as oxygen free radicals), could be involved in the pathogenesis of NSAID-induced G.I. damage. Some compounds that can capture free radicals (aminopyrine, thiourea and its derivative, MK 447) or that inhibit the lipoxygenase pathway (MK 447, salicylazosulfapyridine, BW 755, benoxaprofen) are able to abolish indomethacin-induced G.I. damage. After irradiation with hydroxyl free radicals, indomethacin reacts with them to cause marked G.I. injury, even at a submaximal dose, one poorly ulcerogenic by itself. The above findings suggest that oxygen free radicals are one of the causal factors in the formation of NSAID-induced G.I. side effects
Inhibition of gastric acid secretion by adenosine receptor stimulation in the rat.
No full textThe effects of adenosine and its metabolically stable derivative L-phenylisopropyladenosine (L-PIA), acting mainly on A1 receptors, on gastric acid secretion were studied in the rat. Although inactive by intraduodenal route, subcutaneous adenosine significantly inhibited acid secretion. This inhibition, however, was not dose-dependent. On the contrary, L-PIA was able to decrease dose-dependently acid output by both subcutaneous and intraduodenal route, its ED50 being 0.11 mg/kg subcutaneously and 0.24 mg/kg intraduodenally. The inhibitory effect of L-PIA was reduced by prior administration of theophylline. These results suggest that activation of A1-receptors inhibits acid secretion in the rat
Nitric oxide-releasing NSAIDs, a novel class of safe and effective anti-inflammatory agents
No full textEffects on intestinal microflora, gastrointestinal tolerability and antiinflammatory efficacy of diclofenac and nitrofenac in adjuvant arthritic rats
No full textGastrointestinal safety of NO-aspirin (NCX-4016) in healthy human volunteers: a proof of concept endoscopic study
No full textInteraction of a selective cyclooxygenase-2 inhibitor with aspirin and NO-releasing aspirin in the human gastric mucosa.
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