Perfusion of the proximal small intestine with peptone stimulates gastric acid secretion in man
Isenberg, J.I.; Ippoliti, A.F.; Maxwell, V.L.
Gastroenterology 73(4 Pt 1): 746-752
1977
ISSN/ISBN: 0016-5085 PMID: 892377 Document Number: 115267
The duodenum of 7 normal subjects 47 years old and 7 patients with duodenal ulcer 52 years old was perfused, through a gastroduodenal tube with 2 balloons straddling the pylorus, with 10% peptone solution (w/v, 400 mOs/litre) at 2 ml/min for 4 h. The next day a control test was made with NaCl 0.2 mol/litre. Basal gastric acid secretion was greater in the patients than in normal subjects. Gastric acid secretion increased gradually during duodenal peptone perfusion and was most at 2 h. By the 2nd hour of infusion mean peak 30-min secretory rate was 203.8 plus or minus 31.9 mu Eq/min compared to 87.8 plus or minus 27.2 mu Eq/min with NaCl. The NaCl solution did not stimulate acid secretion. Peak 30-min secretory rate with pentagastrin, 6 mu g/kg bodyweight given subcutaneously and measured on another day, was 657.6 plus or minus 50.6 mu Eq/min. In the periods of peak gastric acid secretion, serum gastrin, measured every 30 min, was unchanged from basal and NaCl control values, but mean serum gastrin increased slightly in all subjects in the last 90 min of duodenal peptone infusion. Validation experiments showed 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 h 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. The findings indicated that there is an intestinal phase of gastric acid secretion in normal men and in patients with duodenal ulcer in response to duodenal peptone perfusion, that the phase has a latent period of about 1 to 2 h until the peak response is reached and that the response is probably not primarily attributable to gastrin release.