Aspects of the effect of metiamide on pentagastrin-stimulated and basal gastric secretion of acid and pepsin in man.
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This study has examined the inhibition produced by metiamide on the gastric secretion of acid and pepsin in 13 patients with duodenal and three with gastric ulcer. The effect of metiamide on the response to a range of doses of pentagastrin in three normal individuals was determined, as was the interaction of metiamide and atropine on prolonged basal secretion. Metiamide inhibited the secretion of acid more than pepsin and the gastric secretion of patients with gastric ulcer more than duodenal ulcer. Metiamide inhibited both the maximal secretory response attainable with pentagastrin and decreased the sensitivity to pentagastrin. Atropine augmented and prolonged the action of metiamide. (+info)
The effect of histamine H2-receptor blockade with metiamide on serum gastrin levels in man.
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Metiamide, an histamine H2-receptor antagonist which inhibits gastric acid secretion, does not lower basal serum gastrin concentration in man. Serum gastrin responses after stimulation by food were marginally higher when the stimulus of food was preceded by metiamide. (+info)
An indirect sympathomimetic effect of burimamide on kitten isolated atria.
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1. Burimamide (34-1080 muM) caused a concentration-dependent increase in the force and frequency of contraction of kitten isolated atria. 2. Metiamide (467 muM) had no stimulant action on kitten atria and did not modify the effects of burimamide. 3. The atrial stimulation produced by burimamide was reduced by (-)propranolol (34-68 nM) and by cocaine (3 muM). 4. The atrial stimulant effect of burimamide was prevented by pretreatment of kittens with reserpine (1 mg/kg, 24 h before the experiment). 5. It is concluded that burimamide causes atrial stimulation by releasing catecholamines. (+info)
An analysis of the depressor responses to histamine in the cat and dog: involvement of both H1- and H2-receptors.
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1 The depressor responses to histamine, in anaesthetized cats and dogs, have been shown to involve both histamine H1- and H2-receptors. 2 In both species, histamine caused dose-dependent falls in blood pressure. The dose-response curve could be displaced to the right by administration of mepyramine 2.5 times 10(-6) mol/kg i.v. The displacement was maximal with a dose-ratio of less than ten. 3 Metiamide alone, up to 2 times 10(-6) mol kg-1 min-1, had no significant effect on the histamine dose-response curve. 4 When administered in the presence of mepyramine, metiamide, 4 times 10(-7) and 2 times 10(-6) mol kg-1 min-1, caused dose-dependent displacements to the right, of the histamine dose-response curve greater than could be achieved with mepyramine alone. 5 The results indicate the presence of both histamine H1- and H2-receptors in the cardiovascular system of the cat and dog. Both receptors produce a common response, i.e. a fall in blood pressure. (+info)
Histamine receptors in peripheral vascular beds in the cat.
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1. The vasodilator activity of histamine has been studied in anaesthetized cats. 2. Histamine causes dose-dependent vasodilatation in the vasculature of the hind-limb and mesentery, perfused with blood at constant flow. 3. Experiments using the selective antagonists mepyramine and metiamide indicate the involvement of both H1- and H2-receptors in the vasodilator responses to histamine. Mepyramine (2.5 X 10(-6) mol/kg), causes displacement of the histamine dose-response curve. This displacement is maximum with a dose-ratio of about 10. Further dose-dependent displacement of the dose-response curve occurred after metiamide (4 X 10(-7) mol kg-1 min-1 and 2 X 10(-6) mol kg-1 min-1), although these doses of metiamide had no effect on histamine responses in the absence of mepyramine. 4. Vasodilator responses could also be elicited by the selective H1-receptor agonists, 2-methylhistamine, 2-(2-aminoethyl)pyridine and 2-(2-aminoethyl)thiazole and the selective H2-receptor agonist, 4-methylhistamine. 5. The selectivity of mepyramine and metiamide as histamine receptor antagonists was confirmed by their failure to reduce the vasodilator responses to acetylcholine, isoprenaline and bradykinin. (+info)
Effect of metiamide on basal and stimulated serum cholecystokinin levels in duodenal ulcer patients.
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Serum cholecystokinin (CCK) levels were measured in 10 patients with chronic duodenal ulcers, fasting and at intervals after two standard tests meals (300 ml of 40 mmol/1 phenylalanine solution), one given before and one during H2-receptor blockade with metiamide (200 mg four times a day). Fasting serum CCK levels were lower in all patients during treatment with metiamide (the mean level falling from 306-0 +/- 102-0 (SEM) to 82-1 +/- 23-6 pg/ml after treatment (p less than 0-01)). In contrast, peak serum CCK levels after the meal were not significantly different (7400 +/- 1141 pg/ml before treatment and 7569 +/- 1293 pg/ml on metiamide). We conclude that in duodenal ulcer patients CCK secretion under basal condtions may be in part dependent on stimulation of the small intestinal mucosa by gastric acid, but that, after an amino acid meal, gastric acid secretion is less important in determining the amount of CCK released. (+info)
Inhibition of gastric secretion in treatment of pancreatic insufficiency.
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The content of pancreatic enzymes in the duodenum was studied in two patients with pancreatic achylia after a standard meal supplemented with commercial pancreatic extract. Gastric transit of the enzymes, with appearance of near-normal amounts in the duodenal contents, occurred only after inhibition of gastric secretion and buffering of residual gastric acid with antacids. Gastric inhibition and neutralisation of acid are therefore necessary for the satisfactory treatment of patients with pancreatic exocrine insufficiency but normal gastric function. (+info)
Effects of metiamide and propranolol on gastric secretion in anesthetized dogs.
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The effects of metiamide, a histamine H2-receptor antagonist, and propranolol, a beta-adrenergic blocking agent, on gastric secretion were studied in anesthetized dogs. Metiamide, 1.45 mg/kg i.v., markedly inhibited the gastric secretion induced by a continuous i.v. infusion of tetragastrin (8 microng/kg-hr), histamine dihydrochloride (160 microng/kg-hr), or methacholine bromide (100 microng/kg-hr). Propranolol 0.5 or 1.0 mg/kg i.v. produced a significant potentiation of tetragastrin-induced gastric secretion but no influence of the secretion induced by methacholine. Propranolol at 5 or 10 mg/kg i.v. produced a slight reduction of the tetragastrin-induced secretion and a significant reduction of methacholine-induced secretion. Histamine-induced gastric secretion was not affected by propranolol at either 1 and 10 mg/kg i.v. These findings lend support to the hypothesis that interactions among histamine, gastrin and acetylcholine receptors do occur though the degree would not be the same in all directions. (+info)