Duodenal acidification inhibits sphincter of Oddi motility in the prairie dog

Recent studies have explored the influence of various hormones, peptides, and neural innervation on the sphincter of Oddi (SO). However, only older and conflicting data are available on the effect of intraduodenal (ID) perfusion of acid on SO activity. Therefore, we tested the hypothesis that acidification of the proximal small bowel would alter SO motility. In acute terminal experiments, 19 adult male prairie dogs underwent cannulation of the gallbladder (GB) with a pressure-monitored perfusion catheter. The common bile duct was cannulated proximally with a drainage catheter and distally with a triple-lumen, side-hole, closed-tip catheter with one port positioned in the SO. The duodenum was cannulated distal to the SO to allow perfusion of the proximal 30 cm of intestine with saline. SO phasic wave frequency (F), amplitude (A), and baseline pressure as well as GB pressure were measured for 40 min prior to and during ID perfusion of saline at pH 8.8, pH 6.0, or pH 2.0. A SO motility index (MI = F × A) was calculated for each 10-min period of the experiment. Infusion of saline at pH 8.8 had no effect on SO function. ID perfusion of saline at pH 6.0 reduced SO MI to 39% (P < 0.05) and 34% (P < 0.05) of control values at 20-30 and 30-40 min, respectively. ID saline at pH 2.0 reduced the SO MI to 51% (P < 0.01) and 53% of control values during the same periods. SO phasic wave frequency was similarly reduced by ID perfusion with saline at pH 6.0 (P < 0.05) and pH 2.0 (P < 0.025). SO phasic wave amplitude, baseline pressure, and GB pressure were unaffected by ID perfusion. These findings indicate that in the prairie dog duodenal acidification inhibits SO activity without affecting GB pressure. This response differs from that observed with exogenous cholecystokinin or motilin infusion but is similar to that observed with intravenous peptide YY in this species.