Basal and stimulated human gastric bicarbonate secretion.
The mucus-bicarbonate barrier on the gastric mucosa is regarded as a first-line of defence against acid. Both mucus and bicarbonate originate from the mucus cells in the gastric mucosa. Bicarbonate is secreted actively by Cl-/HCO3- exchange at the luminal cell membrane. A computer based system with continuous measurement of pH and PCO2 in a gastric perfusion system was used to determine human gastric bicarbonate secretion. The rate of basal gastric bicarbonate secretion in 24 healthy subjects was 386 +/- 31 mumol/h (mean +/- SEM). The 95% confidence interval for basal bicarbonate output was 103-669 mumol/h. Vagal stimulation by sham feeding increased the bicarbonate output by 63% and instillation of 16,16 dimethyl prostaglandin E2 increased the bicarbonate output by 214%. The response to vagal stimulation was independent of intragastric pH. The sham feeding response was abolished by premedication with anticholinergics. Basal and vagally stimulated bicarbonate secretion was unaffected by prostaglandin biosynthesis blockade.
D015064:16,16-Dimethylprostaglandin E2 / Q000494:pharmacology; D000328:Adult; D001639:Bicarbonates / Q000378:metabolism*; D005260:Female; D005753:Gastric Mucosa / Q000187:drug effects / Q000294:innervation / Q000378:metabolism*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D008875:Middle Aged; D014630:Vagus Nerve / Q000502:physiology
D001639:Bicarbonates; D015064:16,16-Dimethylprostaglandin E2