ISSN:
1573-2568
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract In conscious dogs with gastric and duodenal Thomas fistulas, we studied the effect of ethanol on plasma concentrations of gastrin. Ethanol was given either as an infusion into a peripheral vein (1.95 M, 200 ml/hr) or into the duodenum (0.95 M, 400 ml/hr) or as an intragastric bolus injection. The effect of the intragastric bolus injection of 200 ml of different concentrations (0.3 M, 1.7 M, 6.85 M) of ethanol was compared with that of equimolar solutions of urea and sucrose (0.3 M, 1.56 M), and with that of sodium taurocholate (0.06 M) and distilled water. The gastrin responses to an oral mixed-meat meal (35 g/kg) were also investigated. Intragastric bolus injection of isoosmolar *0.3 M) ethanol, but not of equimolar solutions of urea and sucrose or H2O, significantly (P〈0.05) increased plasma gastrin levels above basal. Hyperosmolar solutions of ethanol, urea, and sucrose as well as hypoosmolar sodium taurocholate produced a pronounced increase of plasma gastrin concentrations above basal. The comparison of the mean 2-hr integrated plasma gastrin responses (IRG) showed that ethanol (6.85 M), urea (6.85 M), and sodium taurocholate (0.06 M) are at least as potent stimuli of release of gastrin as the test meal used. Intraduodenal and intravenous infusion of ethanol did not significantly alter mean plasma gastrin concentrations. We conclude that in the dog ethanol, but not urea and sucrose, given in a concentration (0.3 M) which is known not to disrupt the gastric mucosal barrier, increases plasma gastrin levels. This release of gastrin by isoosmolar ethanol is not due to gastric distension and may be a specific effect of ethanol on the gastrin cells. Furthermore, the release of gastrin by hyperosmolar solutions of ethanol, sucrose, and urea is probably a nonspecific effect and due to damage of gastric mucosa. The effect of a hypoosmolar solution of sodium taurocholate, a well-known gastric mucosal barrier breaker, on gastrin release supports this hypothesis.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF01296856
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