INHIBITION OF GASTRIC-EMPTYING BY ACIDS DEPENDS ON PH, TITRATABLE ACIDITY, AND LENGTH OF INTESTINE EXPOSED TO ACID

Exposure of the small intestine to acid inhibits gastric emptying in a dose-related fashion that depends on titratable acidity and pH. Little information is available on the location of this inhibitory mechanism or on the relative contribution of titratable acidity and pH to this feedback control. We hypothesized that the dependence on titratable acidity is related to the length of the intestine exposed to acid and that the dependence on pH is related to the region of the intestine exposed to acid. To test these ideas, we studied 11 dogs with duodenal and jejunal fistulas. The inhibitory effects were tested when different lengths of the small intestine were exposed to test solutions of 0.03, 0.06, and 0.12 meq/ml titratable acidities. pH as an independent covariable was separated from titratable acidity by comparing the inhibition of gastric emptying of lactic acid (pH fixed to 2.4) to HCl (pH 0.96-1.6). Maximal inhibition of gastric emptying by both acids depended on acid exposure of a length of small intestine that was > 65 but less-than-or-equal-to 150 cm long. When acid was confined to the proximal 15 cm, increasing concentration of HCl (decreasing pH) resulted in increasing inhibition, but this effect was absent with increasing concentration of lactic acid (fixed pH). Inhibition was absent when 0.06 meq/ml HCl was infused into the intestine beyond the midintestine. We concluded that 1) the load (titratable acidity)-dependent inhibition of gastric emptying was related to the length of the small intestine exposed to acid, 2) a potent low-pH-sensitive inhibitory mechanism operated independently from titratable acidity in the proximal 15 cm of the duodenum, and 3) the intestinal sensors to acids were only present in the proximal half of the intestine.