J. Dalenback et al., MECHANISMS BEHIND CHANGES IN GASTRIC-ACID AND BICARBONATE OUTPUTS DURING THE HUMAN INTERDIGESTIVE MOTILITY CYCLE, American journal of physiology: Gastrointestinal and liver physiology, 33(1), 1996, pp. 113-122
Human gastric interdigestive acid and bicarbonate outputs vary cyclica
lly in association with the migrating motor complex (MMC). These pheno
mena were studied in 26 healthy volunteers by constant-flow gastric pe
rfusion, with continuous recording of pH and PCO2 in mixed gastric eff
luent and concomitant open-tip manometry of gastroduodenal motility. S
table acid and bicarbonate outputs were registered during less than 50
% of the MMC cycle. Acid secretion started to increase 71 +/- 3% into
the cycle, with maximum output during antral phase III. Bicarbonate ou
tput increased biphasically 1) 40 +/- 5% into the cycle, coinciding wi
th reflux of bile, and 2) at the end of duodenal phase III when the as
pirate was devoid of bile. The bicarbonate peak associated with phase
III was abolished by atropine (0.01 mg/kg iv, n = 8) and by pyloric oc
clusion (n = 9) but remained unchanged after omeprazole (n = 10). The
acid peak was abolished by both atropine and omeprazole. It is conclud
ed that the MMC-related changes in acid and alkaline outputs represent
two different and independent phenomena. Acid secretion cyclicity is
due to periodical variations in cholinergic stimulation of the parieta
l cells. In contrast, the phase III-associated increase in bicarbonate
output is due to duodenogastric reflux.