Gastric CO2 output via the esophagus increases during systemic hypercapnia in anesthetized cat

Abstract

The stomach extracts arterial CO2 during respiratory acidosis to produce HCl & HCO3−, which react in the lumen to re‐form CO2. This study tested the hypothesis that hypercapnia stimulates gastric CO2 removal via the esophagus. Tracheal and esophageal CO2 (PEsCO2) and flows were measured in 13 anesthetized, pyloric occluded cats. Tracheal and gastric CO2 output (V̇ GCO2) and gastric minute ventilation (V̇ G) were calculated during tracheal air breathing for 30min (Control) and CO2 breathing: 10%CO2 in air (1hr), recovery in air (30min), followed by 6×10min alternating paired bouts of 10%CO2 and air (10CO2, 10air). CO2 breathing increased PEsCO2 above control 77% after 1hrCO2 and 123% during 10CO2. Coughing revealed more CO2 was present in the stomach: PEsCO2 increased 134% (in air) and 115% (after 1hrCO2) compared to pre‐cough PEsCO2. V̇ GCO2 ranged from 0–15% (X̄=2.5%) of total CO2 output during 1hrCO2. V̇ G was 27% higher during 10CO2 versus 10air. Relative to control, V̇ G increased 95% after 1 hrCO2 and 148% after the first bout of 10minCO2. The results show a dynamic, supplemental CO2‐eliminating response by the gastroesophageal system during systemic hypercapnia (NIH HL89104, HL103415 & ONR).