Background: Gastric regional CO(2) accumulation indicates gastric mucosal hypoperfusion in critically ill patients. CO(2) is also a reaction product of urea degradation, and we therefore tested the hypothesis if regional pCO(2) 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 microg/kg/h/i.v.) and application of omeprazole (40 mg i.v.).
Results: Gastric regional pCO(2) 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 pCO(2) 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 CO(2) that is suppressed by application of a proton pump inhibitor.
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