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It has been shown that enhanced acid secretion can be suppressed in the rat by systemic administration of glucose. We have recently reported that enhancement of acid secretion as a result of pentagastrin was diminished by intragastric administration of D-glucose. Present study was designed to investigate whether intragastric D-glucose influences gastric acid secretion associated with carbachol and histamine in rat, and then we compared these results with our previous results obtained by pentagastrin-induced hyperacidity. Intravenous infusion of carbachol (1 mg/100 g/h) and histamine (0.5 mg/100 g/h) caused an immediate increase in acid secretion with a peak starting after 40 and 60 min and then reached to a steady state respectively. 1ntragastric administration of D-glucose significantly reduced the hyperacidity induced by histamine and carbachol (p<0.01). The effect of intragastric D-glucose on hyperacidity induced by pentagastrin or histamine when compared with carbachol-induced hyperacidity was significantly greater than carbachol group. In conclusion, it is suggested that the inhibitory effect of intragastric D-g1ucose observed in hyperacidity may be the result of glucose-induced modification of intragastric pathways in parietal cells that control gastric acid secretion.

Keywords: lntragastric D-glucose; Carbachol; Histamine; Gastric acid

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