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[Bicarbonate deficiency and duodenal peptic ulcer]
Terapevticheskii Arkhiv
|April 29, 1998
Summary
Duodenal ulcer patients exhibit reduced gastric bicarbonate secretion, impacting alkaline/acid balance. H2-histamine receptor blockers helped restore this balance, suggesting bicarbonate deficiency in duodenal ulcer pathogenesis.
Area of Science:
- Gastroenterology
- Physiology
Background:
- Alkaline gastric secretion plays a crucial role in maintaining acid-base balance within the stomach.
- Dysregulation of gastric secretion is implicated in the pathogenesis of gastrointestinal diseases like duodenal ulcers.
Purpose of the Study:
- To investigate alkaline gastric secretion in healthy individuals and patients with duodenal ulcers (DU) and chronic gastritis (CG).
- To evaluate the effects of H2-histamine receptor blockers on gastric secretion in these groups.
Main Methods:
- Enrolled 74 DU patients, 28 CG patients, and 16 healthy controls.
- Assessed gastric secretion in basal and hydrochloric acid-stimulated states.
- Administered ranitidine (an H2-histamine receptor blocker) to observe its effects.
Main Results:
- DU patients showed significantly reduced bicarbonate secretion in basal and stimulated conditions.
- A threefold decrease in the alkaline/acid secretion ratio was observed in DU patients, with a trend towards acidosis.
- H2-histamine receptor blocker administration led to the recovery of the acid-alkaline balance.
Conclusions:
- Bicarbonate deficiency is a key pathogenic factor in duodenal ulcers.
- Modulating gastric secretion with H2-histamine receptor blockers can restore acid-alkaline homeostasis.