1,721,040 research outputs found
The beta3-adrenoceptor agonist SR58611A inhibits gastric acid secretion in the conscious cat
No full textNAUNYN-SCHMIEDEBERG'S ARCH.PHARMACOL
Different effects of cimetidine and ranitidine on gastric emptying in rats and man.
No full textCimetidine and ranitidine were tested for their effect on gastric emptying in the rat. At low doses, cimetidine was inactive, whereas it significantly delayed emptying rate when administered at higher doses. Ranitidine always accelerated gastric emptying. At variance with rats, ranitidine delayed human gastric emptying whereas cimetidine was completely inactive. All these data are consistent with the idea that these effects of H2-antagonists are independent of H2-receptor blockade
Different effects of the H2-antagonists on gastric emptying in the rat.
No full textH2-receptor antagonists, in doses capable of inhibiting gastric secretion, did not generally affect gastric emptying. Exceptions were burimamide, which delayed the emptying rate, and ranitidine, which accelerated it. At higher doses burimamide, metiamide cimetidine and oxmetidine delayed gastric emptying, but ranitidine accelerated it to a greater extent. Tiotidine remained ineffective. These data suggest that changes in emptying rate are independent of the H2-receptor blockade
Bombesin delays gastric emptying in the rat.
No full textBombesin, administered by the intraperitoneal route, delayed gastric emptying in conscious rats in a dose-dependent fashion (1--16 microgram/kg). This effect is unlikely to depend on systemic effects of the peptide and is most probably connected with the direct spasmogenic action on the gastroduodenal junction already pinpointed in previous investigations
Histamine H2-antagonists modify gastric emptying in the rat.
No full text1 Histamine H2-receptor antagonists were tested for their effect on gastric emptying in the rat. 2 At low doses all the compounds were inactive except for burimamide which delayed and ranitidine which accelerated gastric emptying. 3 At high doses burimamide, metiamide, cimetidine and oxmetidine delayed, whereas ranitidine accelerated gastric emptying; tiotidine remained ineffective. 4 Changes in emptying rate were not accompanied by changes in emptying pattern which, with all the compounds examined, proceeded, as in the controls, by apparent first order kinetics. 5 The mechanism of the ranitidine-induced acceleration of gastric emptying seemed to be connected with an interference with the cholinergic system, whereas the mechanism of cimetidine- and oxmetidine-induced slowing of gastric emptying was apparently related to cholinolytic and possibly also relaxant effects of the compounds. 6 These different effects of the various H2-blockers are consistent with the idea that changes in emptying rate are independent of H2-receptor blockade
Effect of TRH on pentagastrin-induced gastric acid secretion.
No full textThyrotrophin-releasing hormone (TRH) 20 and 30 micrograms . kg-1 i.v. exerted a moderate inhibition on pentagastrin stimulated gastric secretion in dogs provided with gastric fistula and Heidenhain pouch. The effect was more evident in the main stomach than in the denervated pouch. The inhibitory action of the tripeptide was observed, though to a lesser extent, also in gastric fistula cats, whereas it was completely absent in the anaesthetized rat. Our results showing poor and erratic effects of TRH obtained only with rather high intravenous doses, paralleled those obtained by other authors on gastrointestinal motility and support the suggestion that, if there is a physiological role for TRH in the gastrointestinal tract this is more likely connected with paracrine rather than with endocrine effects of the peptide
(R)-alpha-methylhistamine inhibits ethanol-induced gastric lesions in the rat: involvement of histamine H3 receptors?
No full textThis study examined the gastroprotective effect of (R)-alpha-methylhistamine (MHA), a selective agonist of histamine H-3 receptors, Gastric lesions were induced in the rat by administering absolute ethanol in a volume of 1 ml. Stomachs were removed 1 h later and lesions evaluated both macroscopically and histologically. MHA dose-dependently inhibited ethanol-induced lesions in the range 1-100 mg/kg both by the intragastric and intraperitoneal route. Histological findings indicated that the number of mucous granules in surface and neck cells was increased and the process of reepithelialization was rapidly promoted by MHA. Thioperamide, at 10 mg/kg, inhibited the protective effect of 10 but not of 100 mg/kg of MHA. Larger doses of thioperamide could not be tested because of an interaction with ethanol causing central nervous system effects. Famotidine and indomethacin pretreatment only partially counteracted the MHA effect. The results indicate that MHA is highly effective in preventing ethanol-induced lesions but the exact mechanism is still uncertain
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