Abstract

To determine whether intestinal peptone perfusion stimulates gastric acid secretion in man, the duodenum was infused with 10% peptone (w/v, 400 mOs/1) at 2 ml per min for 4 hr in 7 normal subjects and 7 duodenal ulcer patients. The duodenum was perfused through a gastroduodenal tube which had two balloons straddling the pylorus to present duodenogastric reflux. As a control, 0.2 m NaCl was perfused into the duodenum at 2 ml per min for 4 hr on another day. The order of testing was randomized. Gastric acid secretion increased gradually during duodenal peptone perfusion and reached a peak response during the 2nd hr of infusion. During the 2nd hr of peptone infusion the mean (± se ) peak 30-min secretory rate was 203.8 ± 31.9 μEq per min, and during NaCl infusion it was 87.8 ± 27.2 μEq per min (P se ). Mean (± se ) peak secretory response during the 2nd hr of duodenal peptone perfusion was 32.6 ± 4.6% of the peak response to pentagastrin. During the time periods when gastric acid secretion was at a peak response, serum gastrin, measured at 30-min intervals throughout both tests, was unchanged from basal and NaCl control. However, the mean serum gastrin did increase slightly (approximately 16 pg per ml) but significantly in the 14 subjects during the last 90 min of duodenal peptone perfusion. Validation experiments revealed good reproducibility of the responses to duodenal peptone or NaCl perfusion, absence of an increase in gastric acid secretion or serum gastrin in response to gastric perfusion of 10% peptone in a volume equivalent to the volume which refluxed during the 4 hr of duodenal peptone perfusion, and no effect on gastric acid secretion or serum gastrin of the gastroduodenal tube with or without inflation of the duodenal and gastric balloons. These studies indicate that there is an intestinal phase of gastric acid secretion in normal man and in patients with duodenal ulcer in response to duodenal peptone perfusion, that it has a latent period of about 1 to 2 hr until the peak response is reached, and that the response is probably not primarily attributable to gastrin release.

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