Effects of Metiamide on the Human Stomach

Þjóðleifsson, Bjarni; Wormsley, K. G.

doi:10.1042/cs0490445

Cited by 5 publications

(6 citation statements)

References 20 publications

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“…Our findings of a smaller net H+ flux into the gastric lumen after oral cimetidine compared to controls without significant increase in Na+ flux are consistent with the findings previously reported in man with intravenous metiamide (Thjodleifsson and Wormsley, 1975). Likewise, we have concluded that this reduced value is due to reduction of H+ secretion rather than to increased back diffusion of H+ ions.…”

Section: Discussionsupporting

confidence: 93%

Effect of cimetidine on ion fluxes and potential difference across the human stomach

Ivey¹,

Mackercher²

1978

Gut

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SUMMARY The H2-receptor antagonist, cimetidine, reduces acid output regardless of the means of stimulation. It is not known in man whether this is due entirely to a reduction in acid secretion or whether increased back diffusion of hydrogen ions is also occurring. We studied fluxes of H+, Na+, K+, and Cl -ions after acid instillation into the human stomach in six healthy subjects with and without prior administration of 300 mg cimetidine orally. Potential difference across gastric mucosa was measured continuously throughout each study. Cimetidine caused a significant reduction in hydrogen ion secretion (5 05 mEq per 15 minutes controls versus 2-70 cimetidine, P < 0 05), and consequently a significant reduction in net hydrogen flux into the gastric lumen (2'01 mEq per 15 minutes versus 0-02, P < 0 05). There were no significant differences between sodium ion fluxes in control and cimetidine studies, suggesting that the gastric mucosal barrier remained intact. Cimetidine alone caused a highly significant rise in intragastric pH (to 7) and of potential difference (P < 0 001). Addition of intragastric acid (pH < 1 -0) did not reverse the rise in potential difference caused by cimetidine, suggesting that factors other than change in intragastric pH were involved. In conclusion, our studies support the concept that reduction in acid output by cimetidine is due to inhibition of acid secretion, and not to increased permeability to hydrogen ion.Changes in acid secretion cannot satisfactorily explain gastric mucosal damage associated with conditions such as gastric ulcer or acute aspirininduced mucosal damage. The ill-defined concept of mucosal resistance has long been used to explain such cases. An attempt to define and measure this resistance objectively was the 'gastric mucosal barrier' concept popularised by Davenport (1970); Ivey (1971); Code et al. (1963);and Reitemeier et al. (1957). Davenport found that topical aspirin induced an increase in the net fluxes of Na+ ions into the gastric lumen and at the same time of H+ ions out. Increased net movement of Na+ ions into the lumen and of H+ ions out was termed 'alteration' or 'damage' to the 'gastric mucosal barrier' which limited potentially damaging H+ ion movement into the gastric mucosa. In Davenport's studies, alteration of net Na+ and H+ fluxes was associated with a fall in PD. Other workers (Chvasta and Cooke, 1972) confirmed this, and so changes in PD became "Address for reprint requests: Kevin J. Ivey,

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Section: Discussionsupporting

confidence: 93%

Effect of cimetidine on ion fluxes and potential difference across the human stomach

Ivey¹,

Mackercher²

1978

Gut

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“…The calculations used to determine the secretory response to the Oxo meal and the ionic fluxes following instillation of the acid load into the stomach have been described previously [4]. In studies using marker infusions, to assess completeness of gastric aspiration, corrections were made for transpyloric losses of gastric juice.…”

Section: Calculations and Statistleal Analysesmentioning

confidence: 99%

Effects of a mast cell stabiliser (FPL 52694) on human gastric secretion

et al. 1985

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The effects of a new monochrome mast cell stabilizer (FPL 52694) on gastric secretion have been studied in healthy volunteers. When administered orally for 3 days, FPL 52694 consistently reduced nocturnal and pentagastrin-stimulated secretion of acid by about 50%. Meal-stimulated gastric secretion was not affected by the drug. Inhibition of the gastric secretory response to pentagastrin was not significant when single doses of the drug were administered either into the stomach or the duodenum, but administration of multiple doses resulted in significant inhibition. The drug does not inhibit gastric secretion by injuring the gastric mucosa, since the gastric mucosal barrier to back diffusion of hydrogen ions is not affected. We conclude that this mast cell stabilizer provides an interesting tool for studying aspects of the physiological control of gastric secretion and may have a therapeutic role in peptic ulceration.

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“…Coincident infusion of a different marker into the duodenum also permits estimates to be made of the degree of duodeno-gastric reflux (which may also decrease the amount of acid aspirated from the stomach, as a result of neutralisation by the bicarbonate in the regurgitated duodenal contents). Using this technique, it was demonstrated that metiamide was a true inhibitor of gastric acid secretion (Thjodleifsson & Wormsley, 1975c) but that some prostaglandins reduced the apparent secretion of hydrogen ions by increasing transmucosal loss (O'Brien & Carter, 1975).…”

Section: Mode Of Action Of Antisecretory Drugsmentioning

confidence: 99%

“…Decreased amounts of acid in the gastric aspirate then reflect loss of secreted acid from the luminal contents into the mucosa, rather than inhibition of gastric secretion. The integrity of the gastric mucosal barrier after the administration of antisecretory drugs in man is studied by observing the flux of hydrogen ions and electrolytes out of, and into, the gastric lumen after a solution of known acidity and electrolyte content is introduced into the stomach (Thjodleifsson & Wormsley, 1975c). Such solutions contain an inert marker substance, which allows measurement of the magnitude of 'back diffusion' of acid, as well as loss of instilled solutions into the duodenum and dilution within the stomach.…”

Section: Mode Of Action Of Antisecretory Drugsmentioning

confidence: 99%