Injury of the oesophageal mucosa can result from exposure to refluxed gastric acid and pepsin. Competence

Recent human studies suggest that oesophageal HCO3-secretion, in conjunction with salivary HCO3-secretion and secondary oesophageal peristalsis, is important for the protection of oesophageal mucosa from refluxed gastric contents. This study evaluated simultaneously the responsiveness of oesophageal and salivary HCO3-secretion to oesophageal acidification in eight healthy subjects. A 10 cm segment of oesophagus was perfused at a constant rate of 5 ml/min with a specially designed tube assembly. Saline was used initially, and then 10 mM and 100 mM HCI. The perfusates contained 3H-polyethylene glycol (PEG) as a concentration marker to determine volumes. Corrections were applied for a small degree of contamination by swallowed saliva and refluxed gastric alkali. Oesophageal perfusion with 10 mM HCI did not cause symptoms (nausea and heartburn), but tripled the oesophageal HCO3-output from a baseline of 51 ,umol/10 cm/10 min (p=0.021), while doubling the rate of salivary HCO3 secretion from a median basal value of 140 ,mol/10 min (p=0.021). Oesophageal perfusion with 100 mM HCI was associated with symptoms of nausea and heartburn in all subjects. The median oesophageal HCO3-output increased 32 fold to 1659 gmolJlO cm/10 min (interquartile range 569 to 3373; p=0.036), and salivary HCO3-secretion approximately tripled from basal values (p=0.036). In conclusion, oesophageal acidification stimulates both salivary and oesophageal HCO3-secretion, responses which may be protective to the oesophageal epithelium. (Gu 1995; 36: 649-653)