Tu2001 The Impedance Analysis Using High-Resolution Impedance Manometry Under the 1500 KOhms of Impedance Bar Facilitates Assessment of Pharyngeal Residue in Patients With Oropharyngeal Dysphagia

Abstract

The mechanism by which air distension of the stomach leads to relaxation of the UES is unknown. AIM: To test the hypothesis that transient UES relaxation (TUESR) due to gastric air distension is secondary to activation of esophageal receptors caused by gastric gas escape. Methods: Decerebrate cats (N=10) were implanted with EMG electrodes on the cricopharyngeus (CP) to record UES tone, and a strain gauge on the lower esophageal sphincter (LES) to record LES tone. A gastric fistula was formed for the injection of air or a balloon into the stomach. The effects of the following procedures on gastric distension induced transient relation of the LES (TLESR) and TUESR were tested: gastric balloon distension, restriction of gastroesophageal (GEJ), or venting air from the distal esophagus. RESULTS: We found (N=5) that distension of the stomach with air (mean + SE= 65+ 10 ml) caused TLESR and TUESR. On the other hand, distension of the stomach with up to 150 ml of air in a non-distensible balloon (N=3) activate TLESR, but not TUESR. Restriction of the GEJ during air inflation (75 ml) of the stomach blocked TUESR, but not TLESR (N= 4). Venting the distal esophagus of air prevented air distension induced TUESR (N=3). CONCLUSIONS: TUESR is not related to gastric distension or any reflex associated with gastric distension, it is due gas escaping the stomach during the TLESR. This gas escape stimulates appropriate receptors in the esophagus causing the TUESR. Prior studies have found that air distension of the esophagus activates rapidly adapting mechanoreceptors of the esophageal mucosa activating eructation which includes TUESR.