Nippon Shokakibyo Gakkai Zasshi
Online ISSN : 1349-7693
Print ISSN : 0446-6586
RELEASE OF IMMUNOREACTIVE GASTRIN (IRG) INTO THE DUODENAL LUMEN OF THE DOG
Yuichi MATSUZAWAMichio MIYATAAkiyoshi YOSHIZAWAShintaro ARIMAKyotaro KANAZAWAYasuhiko MORIOKA
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1983 Volume 80 Issue 3 Pages 791-798

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Abstract

We have reported in the previous paper that perfusion of the canine duodenal lumen with the perfusates of pH levels either 1.0 or 3.0 could elicite active release of gastrin into the duodenal lumen from the duodenal mucosa, and gastrin thus liberated was not derived from the mesenteric blood floor.
Basing upon the data mentioned above, we have conducted a series of experiments to check the following points: (1) the molecular components of duodenal luminal gastrin thus obtained and its physiological effectiveness in inducing gastric acid secretion, (2) whether the release of duodenal luminal gastrin being caused by active function of G-cells stimulated by those specific pH levels or merely by destruction of the cells, (3) effectiveness of acetylcholine in inducing duodenal luminal gastrin secretion at various pH levels, and finally (4) effectiveness of the physiological stimuly of ingested food in eliciting duodenal luminal gastrin secretion.
The data and conclusions subsecuently obtained are as the following.
1) The molecular components of duodenal luminal gastrin thus obtained were composed of G-34, G-17, G-14 and the one bigger than G-34, the composition being quite different from the features of plasma gastrin, suggesting the luminal gastrin was directly derived from the duodenal mucosal G-cells. The samples were fully active in inducing gastric acid secretion.
2) The release of duodenal luminal gastrin at active pH levels was reproducible, alternating the pH levels of perfusate from the acidic to neutral then to acidic again. This finding does support the presumption that the release of gastrin at the acidic pH levels is due to the active function of G-cells and not to the destruction of them.
3) Intraluminal application of acetylcholine could release luminal gastrin only at the acidic pH levels, the molecular components thus obtained showed more prominent peaks of big big gastrin and component-I than the samples obtained without the chemical.
4) Perfusing the duodenal lumen with the test meal, we could demonstrate the active release of luminal gastrin even at the more neutral pH levels. The molecular components of luminal gastrin thus obtained were composed of G-34, G-17 and G-14, again different from the features of plasma gastrin.

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© The Japanese Society of Gastroenterology
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