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Biomedical subjects

D C Carter

Publications and source records attributed to D C Carter.

At least 199 records · Page 11Linked to original sources
PubMed1975

Effect of gastric secretory inhibitors on the gastric mucosal barrier.

The effects of the synthetic prostaglandin 16, 16 dimethyl-E2 methyl ester (16-diMe-PGE2) and the histamine H2-receptor antagonist metiamide on the gastric mucosal barrier have been studied using the Heidenhain pouch dog model. The 16-diMe-PGE2 caused significant change in the ionic permeability of the mucosa when instilled into the pouch in a concentration of 300 mug/20 ml. Intravenous administration of 16-diMe-PGE2 did not alter the barrier nor did it alter the response of the mucosa to sodium taurocholate. Metiamide given into the pouch did not affect the mucosa barrier and the response to taurocholate was not affected when metiamide was given locally or intravenously.

Animals↗
PubMed1974

Effect of histamine H2-receptor blockade on vagally induced gastric secretion in man.

Metiamide, an antagonist of histamine H(2) receptors, was administered intravenously to normal subjects and to patients with a peptic ulcer during vagal stimulation with a constant infusion of insulin. In normal and peptic-ulcer subjects there were reductions of 70% and 71% respectively in gastric-acid output compared with control tests on the same subjects. The decreased acid output resulted from a reduction in both volume of secretion and acid concentration. Metiamide is therefore a potent inhibitor of vagally-induced gastric acid secretion.

Adult↗
PubMed1973

Effect of orally administered prostaglandin E 2 and its 15-methyl analogues on gastric secretion.

The effect of orally administered prostaglandin E(2) and its synthetic 15-methyl analogues on gastric secretion in man was studied. The parent E(2) compound did not inhibit basal secretion, whereas both the 15 (S) 15-methyl-E(2) methyl ester and its isomer, 15 (R) 15-methyl-E(2) methyl ester inhibited basal acid secretion. This action is likely to be a direct one on the parietal cell, and it could prove of value in the treatment of peptic ulcer.

Administration, Oral↗
PubMed1973

The gastric secretory response to a continuous insulin infusion in the dog.

The gastric acid response to graded doses of insulin given by continuous infusion was studied in four dogs, each surgically provided with a gastric fistula. All doses of insulin resulted in a prolonged plateau of hypoglycaemia and the degree of hypoglycaemia correlated significantly (p <0.05) with the insulin dose, up to 0.15 u/kg hr. Similarly, graded doses of insulin (up to 0.15 u/kg hr) produced graded acid responses and both the peak acid output and the total acid output correlated significantly with blood glucose changes. No initial inhibitory phase of acid secretion followed the start of the infusion, but a dose-related delay in the onset of the acid response was observed. Our results indicate that insulin provides a quantitative glycopenic stimulus producing a quantitative vagal acid response.

Animals↗