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PubMed1976

Effect of metiamide on basal and stimulated serum cholecystokinin levels in duodenal ulcer patients.

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.

Cholecystokinin↗

PubMed1977

Nocturnal metiamide treatment in the management of healed duodenal ulceration.

This paper presents the results of a pilot study to investigate whether the administration of a nocturnal dose of metiamide (the first orally active H2 receptor antagonist) would prevent or delay the relapse of duodenal ulceration after initial ulcer healing. Sixteen patients took part in a double-blind trial to compare metiamide (400 mg) with placebo. Endoscopically confirmed duodenal ulcer relapses occurred in two out of eight on metiamide and six out of eight on placebo. There was a significant prolongation of remission in those in those on the active drug with an apparent reduction in duodenitis.

Adult↗

PubMed1978

Gastric antisecretory effects of propantheline bromide and metiamide in rhesus monkeys.

The effects of propantheline bromide (PB) and metiamide (M), two dissimilar classes of gastric secretory inhibitors, were studied in chronic gastric fistula rhesus monkeys. Basal and stimulated gastric secretory studies were conducted in conscious monkeys. Multiple s.c. injections of either histamine or pentagastrin were given hourly for four consecutive hours. One hour after the injection of the stimulants a constant plateau of gastric secretion was reached, and the test compounds were then administered as a single i.v. bolus dose. Propantheline bromide at doses of 0.03--0.3 mg/kg inhibited basal and pentagastrin stimulated gastric secretion, but had no effect on histamine stimulation. Total acid output paralleled inhibition of volume of secretion, while there was little or no effect on acid concentration. Metiamide at the doses of 1--10 mg/kg inhibited basal, pentagastrin and histamine stimulated gastric secretion. Metiamide was equally effective in inhibiting the volume of secretion and acid concentration. The scope of the gastric secretory inhibition in the rhesus monkey achieved with these pharmacological agents is very similar to man. These results suggest that the rhesus monkey is an important animal model for predicting clinically useful gastric secretory inhibitors.

Animals↗

PubMed1977

[Evaluation of H2 receptor blockade with metiamide in stress ulcers in rats].

Restrain stress in rats inhibits gastric secretion and microcirculation. Secretion is further inhibited by metiamide, but mucosal blood flow is restored to normal. During stress the ulcer incidence is high, lower with prophylactic administration of metiamide and least with the latter and preserved gastroduodenal acid transit. No therapeutic metiamide effect can be detected.

Aminopyrine↗

PubMed1975

Treatment of duodenal ulcer by metiamide. A multicentre trial.

In a multicentre double-blind trial 68 patients with endoscopically confirmed duodenal ulceration received metiamide (36 patients) or placebo (32 patients) for four weeks. Healing of duodenal ulcers was significantly increased in patients receiving metiamide (67%) compared with those on placebo (25%). There was also an assoicated significant decrease in daytime pain and antacid consumption in those on metiamide.

Antacids↗

PubMed1977

Resistance to blockade of vasodepressor responses to tolazoline by chlorpheniramine and metiamide in rabbit hindlimb vasculature.

In perfused hindquarters of anesthetized rabbits, metiamide alone and a combination of metiamide and chlorpheniramine failed to modify tolazoline-induced depressor responses, indicating a lack of histamine H1 and H2-receptor involvement. Failure of atropine and propranolol to alter tolazoline responses precludes cholinergic and beta-adrenergic mechanisms. On the other hand, graded pressor responses to histamine were reversed to depressor responses by chlorpheniramine, whereas a combination of chlorpheniramine and metiamide completely abolished the effects of histamine. The latter results confirm that in the rabbit hindlimb vasculature histamine H1 and H2-receptors mediate pressor and depressor responses, respectively.

Acetylcholine↗

PubMed1977

Long-term effects and after-effects of treatment of duodenal ulcer with metiamide.

Three therapeutic regimens were investigated to find the best way of treating duodenal ulceration with the histamine H2-receptor antagonist metiamide. Relapse of duodenal ulceration was not prevented by nocturnal administration of metiamide. Recurrence was prevented by continued administration of metiamide for 1 year, but cessation of treatment was followed by rapid relapse or symptomless recurrence of the ulceration. Repeated short courses (1 month) of treatment resulted in slower symptomatic control and more rapid recurrence of the ulceration. The treatment of duodenal ulcer with H2-receptor antagonists requires further investigation.

Clinical Trials as Topic↗

PubMed1986

Orthogonal arrays of particles in the gastric parietal cell of the rat: differences between superficial and basal cells in the gland and after pentagastrin or metiamide treatment.

The basolateral plasma membrane of gastric parietal cells is characterized by the presence of orthogonal arrays of particles revealed by the freeze-fracture technique. These arrays were quantitatively assessed in freeze-fracture replicas of the gastric mucosa at two different levels of the gastric gland and after pentagastrin and metiamide treatment. The arrays were small and scarce in parietal cells located in the upper part of the gland, while they were markedly more abundant in parietal cells situated at the base of the gland. In both superficial and basal cells, the concentration of the arrays was significantly decreased after pentagastrin or metiamide treatment. This decrease was not due to an increase in the surface area of the basal plasma membrane. These results indicate that the concentration of the orthogonal arrays is a distinctive feature between superficial and basal parietal cells and that the arrays can be modulated by parietal cell function.

Animals↗

PubMed1975

The effects of metiamide on the "activity-stress" ulcer in rats.

Forty rats were housed in standard activity wheel cages and fed for only 1 hr per day. The animals were equally divided into 4 groups that received either saline, 12.5 mg/kg, 25.0 mg/kg or 50.0 mg/kg of metiamide, an H2 receptor antagonist, 3 times a day. All animals died within 11 days and all demonstrated significant gastric lesions in the glandular fundus of the stomach. The 50.0 mg/kg dosage group, however, demonstrated significantly fewer ulcers than the saline animals and the lesions that did occur were significantly smaller than those noted in the control animals. Several hypotheses were offered to explain these results which took into account metiamide's effects on gastric secretion and motor activity. It was suggested that secretion of acid may be an important contributing factor in the formation of gastric ulcers in animals subjected to the "activity-stress" procedure.

Animals↗

PubMed1976

Adenylate cyclase of the dog gastric mucosa: stimulation by histamine and inhibition by metiamide.

The activity of the non-stimulated, basal adenylate cyclase of the dog gastric mucosa is reduced by the histamine H2-receptor antagonist metiamide but not by the histamine H1-receptor antagonist mepyramine. Histamine activates the adenylate cyclase only slightly. In the presence of 10(-5) M metiamide a concentration-dependent stimulation of the enzyme by histamine was found. These data indicate that endogenous histamine in dog gastric mucosal homogenate is contributing at least in part to what is measured as "basal" adenylate cyclase activity. This effect is mediated by H2-receptor excitation and in earlier studies has prevented the demonstration of a stimulatory effect of exogenous histamine on this enzyme.

Adenylyl Cyclases↗

PubMed1975

Metiamide in the Zollinger-Ellison syndrome.

The histamine H2-receptor antagonist metiamide is an inhibitor of endogenous and stimulated gastric-acid secretion. It appears to have therapeutic possibilities in duodenal-ulcer disease. Three patients exhibiting the Zollinger-Ellison syndrome have been treated with this drug for six months or more. Rapid symptomatic improvement occurred in each case, followed by ulcer healing. There were also reductions in gastric secretion and consistent changes in the fasting serum-gastrin concentration. On patient relapsed temporarily during therapy. There have been no side effects. It is concluded that, in the short term, metiamide is of benefit in the Zollinger-Ellison syndrome.

Adult↗

PubMed1975

Gastric secretion during anaesthesia and its inhibition by metiamide and other drugs.

The histamine H2-receptor antagonist, metiamide, inhibits the acid gastric secretion produced by chloralose-urethane anaesthesia in dogs carrying gastric cannulae chronically. This secretion is also prevented by atropine and hexamethonium. "Spontaneous" gastric secretion of vagal origin in conscious dogs is also blocked by metiamide.

Animals↗

PubMed1979

Effects of alkyl analogs of histamine and metiamide on gastric acid secretion.

Histamine and metiamide analogs with alkyl, methyl, ethyl or isopropyl groups on the imidazole ring in position 5, not previously tested on an in vivo preparation, were studied for their effects on gastric acid secretion in cats with gastric fistulas. Our findings confirmed that the methyl group appears to be optimal for an effect on gastric acid secretion as regards both agonism and antagonism. Ethyl substitution apparently did not change the pharmacological activity of histamine but modified the inhibitory effect of metiamide from competitive to non-competitive kinetics. Isopropyl analogs were inactive on gastric secretion under our experimental conditions.

Animals↗

PubMed1976

Treatment of stress-induced upper gastrointestinal/hemorrhage with metiamide.

The H-2-blocking antihistamine metiamide was used to treat 14 episodes of bleeding from the stomach or duodenum in eleven patients. In 11 instances bleeding was due to erosive gastritis or duodenitis and bleeding promptly ceased after one or two doses of 300 mg at 6 h intervals and did not recur as long as the drug was continued. In the 2 instances in which bleeding continued, chronic ulcers had eroded into major blood-vessels. There were no complications from the drug even in five patients with severe bone-marrow suppression after renal transplantation. Metiamide seems to be a safe and highly effective agent in the control of bleeding due to erosive gastritis.

Adolescent↗

PubMed1975

The effects of burimamide and metiamide on basal gastric function in the cat.

1 Burimamide injected intravenously in the anaesthetized or conscious cat produced significant increases in gastric acid secretion: in the anaesthetized cat it produced increased gastric mucosal blood flow. 2 Metiamide, in doses which inhibited pentagastrin-stimulated acid secretion, produced no increase in gastric acid secretion in conscious animals, or gastric acid secretion or gastric mucosal blood flow in the anaesthetized cat. 3 Metiamide did not influence the amount of acid which diffused out of the stomach when instilled at pH values between 1.5 and 6.0. 4 The possible mode of action of burimamide in increasing basal gastric secretion is discussed.

Anesthesia↗

PubMed1976

The effect of metiamide on acid secretion stimulated by gastrin, acetylcholine and dibutyryl cyclic adenosine 3',5'-monophosphate in the isolated whole stomach of the rat.

1 An isolated stomach preparation from immature rats is described. The lumen of the stomach was perfused and the hydrogen ion activity of the perfusate recorded continuously. 2 The preparation gave dose-dependent responses to gastrin, acetylcholine and dibutyryl cyclic adenosine 3',5'-monophosphate and these responses were readily reversed on washing out the agonist. 3 The acid secretory response to gastrin was inhibited by metiamide at concentrations of 10(-5) M and 3 X 10(-5)M. 4 The acid secretory responses to acetylcholine and dibutyryl cyclic adenosine 3',5'-monophosphate were not inhibited by concentrations of metiamide up to 10(-3) M. 5 These findings are discussed in relation to the role of histamine in the control of gastric acid secretion.

Acetylcholine↗

PubMed1984

Effects of the anti-inflammatory agents indomethacin, metiamide and acetylsalicylic acid on the induction of hyperplasia in hamster cheek-pouch epithelium and ear epidermis.

Previous studies have shown that agents such as indomethacin and hydrocortisone act to reduce the level of epidermal hyperplasia produced by various chemical, but little information is available about the effects of such anti-inflammatory agents on the induction of hyperplasia in oral mucosa. Hamster cheek-pouch epithelium and ear epidermis were treated with indomethacin, metiamide and acetylsalicylic acid prior to treatment with turpentine, podophyllin or TPA. The levels of hyperplasia induced were monitored by rates of epithelial glycolysis, protein synthesis and mitosis. The response of the metabolic assays to epinephrine was also examined. Alone, turpentine, podophyllin and TPA each caused a 3-5 fold increase in the metabolic assays and loss of the normal tissue response to epinephrine. Tissues pretreated with indomethacin showed significant reductions in the levels of hyperplasia produced and they retained a normal response to epinephrine. No reduction in hyperplasia was observed following pretreatment with acetylsalicylic acid, an alternative inhibitor or prostaglandin synthesis or with metiamide, a histamine blocker. The results indicate that the production of epithelial hyperplasia by turpentine, podophyllin and TPA can be inhibited by indomethacin.

Animals↗

PubMed1976

Effect of the H2-receptor antagonist metiamide on carbachol- and histamine-induced gastric acid secretion in the Atlantic cod,Gadus morhua.

Gastric acid secretion was measured in swimming codfish surgically equipped with a catheter draining the stomach. Intramuscular injection of histamine (15.6 mug/kg-h) or carbachol (5 mug/kg-h) stimulated the secretion of acid, carbachol in addition caused a marked decrease in drinking rate of the fishes. Administration of 10 mumol/kg-h metiamide completely prevented the acid secretion induced by both drugs. The carbachol effect on the drinking rate, interpreted to mirror contraction of the stomach following stimulation of muscarinic receptors, was not affected by metiamide.

Animals↗