The acid-removing capability of the duodenal mucosa itself, without the secretions of Brunner's glands, the pancreas, or liver, has recently become recognized. Whether this acid loss occurs by a backdiffusion of hydrogen ion, bicarbonate neutralization, a combination of the above two processes, or some other mechanism, remains unclear. Experiments were carried out in dogs with chronic distal duodenal pouches or with gastric fundal pouches. Acid loss and CO2 levels were measured simultaneously in situ. The hypothesis was that, if bicarbonate neutralization of acid was going on, CO2 would appear in the pouches as a result of the reaction H+ + HCO3 → H2O + CO2. In the duodenal pouches, Pco2 did rise as acid was lost. For 22 experimental observations, the net acid loss from the pouches (JH+) correlated directly and significantly with pouch Pco2 generation according to the equation JH+ = 7.6 Δ Pco2 + 75 (r = 0.79, P<0.001). By contrast Pco2 levels were not increased in dogs with gastric pouches when the 'barrier' was broken and acid loss occurred. When the system was run with a plastic cannula replacing the duodenal mucosal pouches and bicarbonate was infused to simulate the rates of acid loss seen in the duodenum, Pco2 levels in the plastic cannulas were similar to those seen in vivo. We, therefore, conclude that bicarbonate neutralization is responsible, at least in part, for acid loss in isolated canine duodenal loops.
|Original language||English (US)|
|Journal||American Journal of Physiology Endocrinology Metabolism and Gastrointestinal Physiology|
|State||Published - 1978|
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