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At least 73 records · Page 4Linked to original sources
PubMed1975

Relief of duodenal ulcer sysmptons by oral metiamide.

Thirty patients with symptoms of duodenal ulceration were treated for five to eight weeks in a double-blind trial with either metiamide 1 g daily by mouth or a placebo. In the 15 patients receiving metiamide there were significant reductions in nocturnal pain and antacid consumption. Daytime pain was diminished. The results suggest that histamine H2-receptor antagonists are likely to be useful in the medical management of the symptoms of duodenal ulceration.

Administration, Oral↗
PubMed1980

Inhibition of gastric acid secretion in the dog by the H2-receptor antagonists, ranitidine, cimetidine, and metiamide.

The new H2-receptor antagonist, ranitidine, has been compared with cimetidine and metiamide as an inhibitor of gastric acid secretion in the dog. All three compounds were effective both intravenously or by mouth in inhibiting secretion induced by histamine, pentagastrin, or bethanechol. This inhibition was mainly attributable to a reduction in the volume of secretion, although there was also a significant reduction in the concentration of acid secreted. Metiamide was slightly less active than cimetidine, but ranitidine was four to nine times more potent than cimetidine, depending on the secretagogue used. The antisecretory activity of ranitidine does not result from a limitation in blood flow to the gastric mucosa.

Animals↗
PubMed1975

Effect of metiamide on acid secretion from isolated kitten fundic mucosa.

Isolated kitten fundic mucosa demonstrates low rates of spontaneous acid secretion in vitro when bathed in Krebs-Henseleit solution, and responds consistently to histamine, pentagastrin, and acetylcholine placed in the bath. High rates of spontaneous secretion or secretion in response to histamine and pentagastrin were significantly inhibited by addition of metiamide (5 X 10(-3) M); but mucosa stimulated by constant addition of acetylcholine chloride (10(-4) M) was not inhibited by metiamide at the same concentration.

Acetylcholine↗
PubMed1981

Effects of alkyl analogues of histamine and metiamide on the isolated guinea pig heart.

The effects of some substitutions in position 5(4) of the imidazole ring in the histamine and metiamide molecule were studied by means of isolated heart preparations from the guinea pig (atria and papillary muscle). Among the histamine analogues 5-methyl and 5-ethyl histamine were found to possess approximately the same intrinsic activity as histamine whereas 5-isopropylhistamine was shown to be absolutely inactive. Among the metiamide analogues the 5-ethyl derivative (etiamide) was found less effective than the parent substance but showed the same kind of competitive antagonism; the isopropyl derivative (isopropiamide) was found to be inactive up to a concentration of 3 X 10(-5) mol/l and to exert a non-competitive antagonism with 3 X 10(-4) mol/l. On the whole the atria and the papillary muscle preparations behaved quite similarly in regard to both the agonistic and the antagonistic compounds.

Animals↗
PubMed1975

Effects of long-term treatment with metiamide.

Metiamide was given to patients with peptic ulcer or oesophagitis in a pilot study to establish the therapeutic value of the drug. Administration of metiamide resulted in relief of pain within a week in the majority of patients. Healing of duodenal and gastric ulcers was observed.

Duodenal Ulcer↗
PubMed1977

Metiamide treatment in five patients with Zollinger-Ellison syndrome.

Five patients with Zollinger-Ellison syndrome received metiamide per os in doses ranging from 600 to 1,200 mg/day for a minimum period of 2 weeks. Drug produced an inhibition of basal gastric acid secretion ranging from 5 to 100% with relief of symptoms. Survey of patients during and after metiamide course showed sometimes a prolonged antisecretory effect up to 26 days after the end of treatment or, on the contrary, a reduced drug activity in spite of increasing doses.

Adult↗
PubMed1977

Effects of metiamide and propranolol on gastric secretion in anesthetized dogs.

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.

Animals↗
PubMed1985

Antagonism of hypotensive and bradycardic effects of centrally administered guanfacine by metiamide in anesthetized rabbits.

In anesthetized rabbits, intracerebroventricular (ICV) administration of the alpha-adrenoceptor agonist, guanfacine, like clonidine, elicited dose-related falls in arterial blood pressure and heart rate. ICV pretreatment with the histamine H2-receptor antagonist, metiamide, significantly reduced the hypotensive and bradycardic responses caused by ICV injection of either guanfacine or clonidine. The present results seem to indicate that the antagonistic effect of metiamide against either guanfacine or clonidine is probably due to its alpha-adrenoceptor blocking action rather than its histamine H2-receptor blocking action, suggesting that these interactions might be of central origin.

Adrenergic alpha-Agonists↗
PubMed1976

Clinical experience with metiamide.

The new histamine H2-receptor antagonist, metiamide, was shown to inhibit acid and pepsin secretion in gastric secretion studies performed on patients suffering from peptic ulceration. The new drug was administered intravenously in these experiments, but effective plasma levels could also be produced by oral administration. When symptomatic patients were treated with the drug nearly all experienced marked symptomatic relief, and there was some evidence that ulcer healing occurred during treatment. When the drug was withdrawn symptoms tended to return. No toxic reactions were encountered in this trial. Double-blind studies are now being made in Britain to establish the place metiamide may have in the treatment of duodenal ulceration.

Depression, Chemical↗
PubMed1977

The in vitro effects of histamine and metiamide on neutrophil motility and their relationship to intracellular cyclic nucleotide levels.

Histamine at concentrations of 1 x 10(-5) M to 5 x 10(-5) M consistently increased neutrophil movement as measured in Boyden chambers. This effect was entirely caused by stimulation of chemokinesis (stimulated random migration) and true chemotaxis was inhibited by these concentrations. This inhibition of chemotaxis could be abolished by pretreatment with metiamide, an H-2 receptor antagonist, and levamisole, but not by diphenylhydramine, an H-1 receptor antagonist. Metiamide at similar concentrations produced a mild stimulation of chemokinesis but has no effect on true chemotaxis. The histamine effects on neutrophil motility were associated with increased levels of intracellular cAMP wehreas cAMP levels were unaffected. Agents known to elevate intracellular cAMP levels produced effects on neutrophil motility similar to those of histamine. It is suggested that histamine exerts a 2-fold effect on neutrophil motility mediated via an H-2 receptor site and associated with elevated levels of cAMP.

Cell Movement↗
PubMed1979

The effect of prostaglandin E2, 15-methyl prostaglandin E2, and metiamide on established canine gastric mucosal barrier damage.

The ability of two types of gastric acid inhibitor to reverse established gastric mucosal barrier damage was studied in canine Heidenhain pouches. A model of established barrier damage was prepared and validated by perfusing Heidenhain pouches with an acid saline solution containing 20 mmoles of aspirin for 2 hours (damage period) and then perfusing with acid saline alone for a third hour (recovery period). Increases in gastric mucosal permeability to H+ and Na+ produced in the damage period still were present and were significant in the recovery period. In subsequent experiments the effect of topically applied prostaglandin E2 and 15-methyl prostaglandin E2 and intravenously administered prostaglandin E2, 15-methyl prostaglandin E2, and Metiamide on the recovery period permeability was studied. Topical application of the prostaglandins and intravenous Metiamide had no effect on the increased permeability. Intravenously administered prostaglandins returned the permeability to normal and therefore reversed established barrier damage. This effect may have important therapeutic implications in acute gastric mucosal lesions.

Administration, Topical↗
PubMed1974

Gastric response to metiamide.

Metiamide greatly reduced pentagastrin-stimulated and overnight secretion of acid and pepsin in 11 patients with duodenal ulcer and virtually abolished gastric secretion in three patients with gastric ulcer. The drug was equally effective when infused intravenously or intraduodenally. A therapeutic trial of Metiamide is warranted in diseases caused or aggravated by excess gastric secretion of acid and pepsin.

Atropine↗
PubMed1975

Relations between the effects of histamine, pheniramin and metiamide on spontaneous motility and the formation of cyclic AMP in the isolated rat uterus.

Histamine (5 X 10(-6) to 10(-3) M) depressed the spontaneous motility of the isolated rat uterus in a dose-dependent manner. Under these conditions uterine cyclic AMP was raised up to 92%. Both effects, uterine relaxation and cyclic AMP accumulation after 2 min could be inhibited dose dependently by the H2-antihistaminic compound metiamide (1.7 X 10(-6) M to 1.7 X 10(-4) M). By contrast, the H1-antagonist pheniramin (4.4 X 10(-5) M) was ineffective. It was concluded that the histamine-induced inhibition of rat uterine motility is mediated by cyclic AMP which is formed in response to stimulation of H2-histaminergic receptors.

Animals↗
PubMed1977

Analysis of the actions of cimetidine and metiamide on gastric acid secretion in the isolated guinea pig gastric mucosa.

Cumulative dose-response curves for histamine were determined on acid secretion from the isolated guinea pig gastric mucosa. Two H2-receptor antagonists-metiamide and cimetidine-behaved like competitive antagonists to histamine on gastric acid secretion in vitro. The isolated guinea pig gastric mucosa seems to be a suitable in vitro model for analysing the action of compounds on receptors involved in acid secretion.

Animals↗
PubMed1975

Early clinical experience with metiamide, a histamine H2-receptor antagonist, in patients with duodenal ulcer.

The clinical, endoscopic, and biochemical effects of metiamide, a histamine H2-receptor antagonist, in therapeutic dosage have been studied in a 28-day open trial in patients with duodenal ulcer disease. A good symptomatic response, combined with a 72% ulcer healing rate was observed. There were small but significant rises in plasma creatinine, serum glutamic oxaloacetic transaminase, and serum lactate dehydrogenase during treatment. Small quantities of amino acids appeared in the urine, and the heart size increased slightly. It is concluded that histamine H2-receptor antagonism may be an important therapeutic approach to duodenal ulcer disease.

Adult↗
PubMed1982

Pharmacological interactions between ranitidine, cimetidine, metiamide and tiotidine at histamine H2-receptor sites in guinea-pig atria.

Cumulative concentration-response curves to histamine or dimaprit were constructed on guinea-pig isolated right atria and agonist dose-ratios were determined following addition of ranitidine, cimetidine, metiamide or tiotidine alone or a combination of any two of these H2-receptor blocking drugs. The observed histamine or dimaprit dose-ratios for combinations of any two of the H2-antagonists tested were consistent with results predicted from the equation, DR1+2 = DR1 + DR2 - 1, for two antagonists competing for the same receptor sites. Therefore we conclude that all four H2-antagonists compete for the same histamine H2-receptor.

Animals↗
PubMed1977

Acute erosive gastritis induced by aspirin, ketoprofen, ibuprofen, and naproxen: its prevention by metiamide and cimetidine.

Aspirin, ketoprofen, ibuprofen, and naproxen all produced acute gastric erosions in rats. Aspirin produced significantly more erosions than ketoprofen, ibuprofen, or naproxen. There was no significant difference between the effects of ketoprofen, ibuprofen, and naproxen. Aspirin and naproxen produced a synergistic effect at higher dosage. Metiamide and cimetidine were effective in preventing this type of experimental acute erosive gastritis.

Acute Disease↗