Gastric luminal somatostatin secretion of normals and patients with pernicious anemia and with Zollinger-Ellison syndrome.
We studied the release of gastric luminal somatostatin-like immunoreactivity (SLI) in response to a pentagastrin infusion (0.9 microgram/kg/hr, intravenous) in five normal volunteers, five patients with pernicious anemia, and two patients with Zollinger-Ellison syndrome. In addition, we studied the gastric luminal SLI secretion in response to a gastric luminal acid perfusion in two patients with pernicious anemia. Our results have shown that: (1) pentagastrin caused a parallel increase in luminal hydrogen ions and SLI release in normal volunteers; (2) Zollinger-Ellison patients had elevated basal acid and SLI levels that did not increase further with pentagastrin; (3) pentagastrin did not increase gastric acid or luminal SLI secretion in pernicious anemia patients; and (4) in pernicious anemia patients, a gastric luminal acid perfusion caused a significant increase in gastric luminal SLI over baseline values. In conclusion, gastric luminal hydrochloric acid appears to be a factor which stimulates the secretion of luminal SLI in human beings.
Ertan
A
A
Department of Medicine, Tulane University Medical School, New Orleans, Louisiana 70112.
Ozden
A
A
Golodner
E
E
Degertekin
H
H
Arimura
A
A
D000328:Adult; D000752:Anemia, Pernicious / Q000378:metabolism*; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010418:Pentagastrin; D013004:Somatostatin / Q000378:metabolism*; D015043:Zollinger-Ellison Syndrome / Q000378:metabolism*
D013004:Somatostatin; D010418:Pentagastrin