Dean & Putnam have postulated a chemosensitive vagovagal-mediated gastroesophageal reflex for CO2 elimination that is controlled by the caudal solitary complex (cSC; Resp Physiol & Neurobiol 173:274, 2010). In the absence of food, respiratory acidosis stimulates cSC neurons resulting in increased gastric blood flow and consumption of arterial CO2 for production of HCl & HCO3−. Intragastric CO2 is reconstituted from luminal H+ & HCO3−, ventilated into the pharynx, and exhaled with pulmonary gas. To test this hypothesis, we measured gastroesophageal CO2 output in anesthetized spontaneously breathing cats. Air or 10%CO2 in air was inspired by tracheal tube for 60min while measuring esophageal CO2 (ESCO2) output below the upper esophageal sphincter (UES). At end-tidal CO2 (ETCO2)=35–45mmHg, adding a 1-way valve or 25cc dead space to the esophagus increased ESCO2 from ≤3 to 15–35mmHg. Activation of cough increased ESCO2 to ≤40mmHg. With the pylorus occluded, raising ETCO2 to 77–85mmHg increased intragastric pressure, esophageal gas flow, ESCO2 (≤80mmHg), and EMG activities of the crural diaphragm (inspiratory) and UES (expiratory) in parallel with increased pulmonary ventilation. ESCO2 usually exceeded ETCO2 during and following cough or spontaneous ‘eructation’ in the post-CO2 period. We conclude that expired CO2 contains gastric CO2 plus alveolar CO2 during respiratory acidosis (NIH HL89104, ONR).