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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Carbon Dioxide, Duodenum, Enzyme Inhibitors, Hydrochloric Acid, Hydrogen-Ion Concentration, Indomethacin, Intestinal Mucosa, Kinetics, Male, Nitric Oxide Synthase, Nitroarginine, Rats, Rats, Sprague-Dawley, Sodium Chloride, Time Factors.
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Does carbon dioxide mediate duodenal mucosal alkaline secretion in response to luminal acidity in the anesthetized rat? Context: Acid exposure of the duodenum elicits various functional responses, e.g., an increased mucosal alkaline secretion. Despite low pH in luminal contents, the mucosal secretion of bicarbonate-rich fluid results in pH neutrality at the surface epithelium. It follows that it is probably not luminal pH that triggers the secretory response. The present study was undertaken to investigate if CO2 could serve as an intermediate messenger between luminal acid and the mucosal secretory response. Experiments were performed on chloralose-anesthetized rats. The duodenal mucosal alkaline secretion was measured by in situ pH-stat titration. Exposure of the duodenal mucosa to CO2, administered either as a pregassed solution (pH 4, PCO2 700 mm Hg) or as an acidified bicarbonate solution (pH 6.4, PCO2 240 mm Hg), raised the alkaline output by approximately 65%. This response was blocked by the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (0.3 mmol/L intraluminally) but not by indomethacin (5 mg/kg intravenously).
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Exposure of the duodenal mucosa to solutions with high concentrations of CO2 increases the mucosal alkaline secretion despite an almost neutral pH. Data indicate that the L-arginine/NO pathway is involved in the mediation of this response. Final Decision: yes