Does Antral Distension Inhibit Gastric Acid Secretion or Stimulate Bicarbonate Secretion in ‘Healthy’ Subjects?
Autor: | A. Hamlet, Lars Fändriks, Jan Dalenbäck, L. Olbe |
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Rok vydání: | 1993 |
Předmět: |
Adult
Male medicine.medical_specialty Bicarbonate Distension Biology Catheterization Helicobacter Infections Gastric Acid chemistry.chemical_compound Parietal Cells Gastric Internal medicine Pyloric Antrum medicine Humans Secretion Intubation Gastrointestinal Aged Helicobacter pylori Stomach digestive oral and skin physiology Gastroenterology Bicarbonate transport Middle Aged biology.organism_classification Pentagastrin Bicarbonates medicine.anatomical_structure Endocrinology chemistry Duodenal Ulcer Gastric acid Female medicine.drug |
Zdroj: | Scandinavian Journal of Gastroenterology. 28:999-1004 |
ISSN: | 1502-7708 0036-5521 |
DOI: | 10.3109/00365529309098299 |
Popis: | The effects of a 150-ml antral balloon distension on pentagastrin-stimulated gastric acid secretion and bicarbonate secretion were studied in nine healthy subjects and eight duodenal ulcer (DU) patients. The gastric secretions were simultaneously measured, using a luminal perfusion and pH/PCO2 measurements. Two of the healthy subjects and six of the DU patients were positive for Helicobacter pylori. When H. pylori-positive and -negative subjects were compared, basal gastric acid and bicarbonate outputs did not differ significantly. In H. pylori-infected subjects the bicarbonate transport increased by about 70% on pentagastrin stimulation. In the H. pylori-negative group pentagastrin had no effect on the bicarbonate secretion. Antral distension elicited a 30-35% inhibition of pentagastrin-stimulated gastric acid secretion in the group of H. pylori-negative subjects, whereas the acid secretory level remained essentially unchanged in the positive group. Bicarbonate secretion decreased transiently by the distension in the negative subjects, whereas a slight increase was observed in the infected group. We conclude that antral distension inhibits pentagastrin-stimulated gastric acid output in healthy H. pylori-negative subjects. Our results strongly suggest that the underlying mechanism is a direct inhibition of gastric parietal cell function and not an increased gastric bicarbonate secretion. Furthermore, the results indicate that this defective distension-induced acid inhibition may be correlated to H. pylori infection rather than to duodenal ulcer disease. |
Databáze: | OpenAIRE |
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