Gastric PCO2 Tonometry Is Independent of Carbonic Anhydrase Inhibition

Tonometric measurement of an elevatedintragastric PCO 2 and a decreased calculatedgastric intramucosal pH can be used to detect gastricmucosal ischemia, provided that intraluminal productionof CO 2 through acid buffering by bicarbonate is avoided byadequate acid secretion suppression. If the diffusionrate is known, steady state PCO 2 can becalculated when measurement intervals are used that areshorter than needed for complete equilibration. TheCO 2 diffusion might be influenced by thechoice of acid-suppressive drugs, since some of theminhibit gastric carbonic anhydrase (CA) and CAfacilitates diffusion of CO 2 /bicarbonate over thegastrointestinal mucosa. We therefore performed gastricPCO 2 tonometry, using acidsuppressiveregimens with and without CA inhibition. The diffusionrate of CO 2 in a gastric tonometer was studied in healthy volunteers,following intravenously administered ranitidine (groupI, N = 8) or ranitidine plus pirenzepine (group II, N =12), a muscarinic antagonist with CA inhibitingcapacities. Measurement intervals were 10, 20, 30 and 60min. Neither the diffusion rate of CO 2 (k =0.13 ± 0.02/min in group I and 0.11 ±0.02/min in group II), nor the steady-statePCO 2 (38 ± 3 mm Hg in group I and 40± 4 mm Hg in group II), nor the gastric- blooddifferences in PCO 2 and pH differed betweengroups. These results indicate that diffusion ofCO 2 into the tonometer balloon is independentof CA and thus of the type of gastric acid secretioninhibition.