A new concept in central CO 2 chemoreception and pH regulation: gastric CO 2 ventilation supplements alveolar ventilation during hypercapnia in anesthetized spontaneously breathing cat

Dean & Putnam have postulated a chemosensitive vagovagal‐mediated gastroesophageal reflex for CO 2 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 CO 2 for production of HCl & HCO 3 − . Intragastric CO 2 is reconstituted from luminal H + & HCO 3 − , ventilated into the pharynx, and exhaled with pulmonary gas. To test this hypothesis, we measured gastroesophageal CO 2 output in anesthetized spontaneously breathing cats. Air or 10%CO 2 in air was inspired by tracheal tube for 60min while measuring esophageal CO 2 (ESCO 2 ) output below the upper esophageal sphincter (UES). At end‐tidal CO 2 (ETCO 2 )=35–45mmHg, adding a 1‐way valve or 25cc dead space to the esophagus increased ESCO 2 from ≤3 to 15–35mmHg. Activation of cough increased ESCO 2 to ≤40mmHg. With the pylorus occluded, raising ETCO 2 to 77–85mmHg increased intragastric pressure, esophageal gas flow, ESCO 2 (≤80mmHg), and EMG activities of the crural diaphragm (inspiratory) and UES (expiratory) in parallel with increased pulmonary ventilation. ESCO 2 usually exceeded ETCO 2 during and following cough or spontaneous ‘eructation’ in the post‐CO 2 period. We conclude that expired CO 2 contains gastric CO 2 plus alveolar CO 2 during respiratory acidosis (NIH HL89104, ONR).