Recent human studies suggest that oesophageal HCO3- secretion, in conj
unction with salivary HCO3- secretion and secondary oesophageal. peris
talsis, is important for the protection of oesophageal mucosa from ref
luxed gastric contents. This study evaluated simultaneously the respon
siveness of oesophageal and salivary HCO3- secretion to oesophageal ac
idification in eight healthy subjects. A 10 cm segment of oesophagus w
as perfused at a constant rate of 5 ml/min with a specially designed t
ube assembly. Saline was used initially, and then 10 mM and 100 mM HCl
. The perfusates contained H-3-polyethylene glycol (PEG) as a concentr
ation marker to determine volumes. Corrections were applied for a smal
l degree of contamination by swallowed saliva and refluxed gastric alk
ali. Oesophageal perfusion with 10 mM HCl did not cause symptoms (naus
ea and heartburn), but tripled the oesophageal HCO3- output from a bas
eline of 51 mu mol/10 cm/10 min (p=0.021), while doubling the rate of
salivary HCO3- secretion from a median basal value of 140 mu mol/10 mi
n (p=0.021). Oesophageal perfusion with 100 mM HCl was associated with
symptoms of nausea and heartburn in all subjects. The median oesophag
eal HCO3- output increased 32 fold to 1659 mu mol/10 cm/10 min (interq
uartile range 569 to 3373; p=0.036), and salivary HCO3- secretion appr
oximately tripled from basal values (p=0.036). In conclusion, oesophag
eal acidification stimulates both salivary and oesophageal HCO3- secre
tion, responses which may be protective to the oesophageal epithelium.