Influence of <i>Helicobacter pylori</i> Infection and Omeprazole Treatment on Gastric Regional CO₂

Abstract

Background: Gastric regional CO₂ accumulation indicates gastric mucosal hypoperfusion in critically ill patients. CO₂ is also a reaction product of urea degradation, and we therefore tested the hypothesis if regional pCO₂ is influenced by Helicobacter pylori infection. Material: Seven H. pylori-positive and 7 H. pylori-negative volunteers (age range 21–30 years) were investigated. During a 6- to 7-hour observation period, we obtained every 30 min arterial blood gases, gastric juice pH from a glass pH electrode and regional pCO2 from a gastric tonometer. The study protocol included subsequent periods of baseline measurements, pentagastrin stimulation (0.6 µg/kg/h/i.v.) and application of omeprazole (40 mg i.v.). Results: Gastric regional pCO₂ was increased in H. pylori-positive versus H. pylori-negative subjects before (64.4 ± 3.1 vs. 50.0 ± 2.9 mm Hg, p < 0.005) but not after application of omeprazole. The effect of omeprazole on gastric juice pH was increased in H. pylori-positive subjects (mean pH during 4 h 6.1 ± 0.3 in H. pylori-positive vs. 2.5 ± 0.2 in H. pylori-negative subjects; p < 0.0001). There was a difference in arterial pCO₂ between H. pylori-positive and H. pylori- negative subjects (43.1 ± 0.3 versus 38.9 ± 0.3 mm Hg; p < 0.0001). Conclusion:H. pylori infection has a significant effect on gastric regional CO₂ that is suppressed by application of a proton pump inhibitor.

Stimulation of growth of the human gastric pathogen Helicobacter pylori by atmospheric level of oxygen under high carbon dioxide tension

“…Hp generates additional CO 2 via the breakdown of urea, thereby increasing bicarbonate levels. In fact, the gastric CO 2 levels in Hp -positive volunteers were significantly higher than those of Hp -negative subjects [67]. The affinity for CO 2 may thus be related to its ecological niche, which may have lead to adaptation and eventually dependency on high CO 2 concentrations.…”

Effect of various test meals on gastric and jejunal carbon dioxide: A study in healthy subjects

“…The analysis of the relation between the remaining acid concentration (and hydrogen ion amount) and the PCO 2 profiles of both the stomach and jejunum showed a poor correlation in both per-subject and group analyses. Other possible explanations of these peaks, such as the presence of gastric H. pylori infection and actual gastric ischemia by vascular stenosis, were excluded [23]. Other explanations could be bicarbonate production by the salivary glands or esophagus and (duodenogastric) reflux.…”