Site of the abnormal stimulus of gastric secretion after small bowel exclusion

Abstract

SUMMARY In dogs with either vagally innervated or denervated pouches, the acid responses to a standard meal, a meal which bypassed the greater part of the small bowel, and a meal introduced directly into the small intestine were measured before and after exclusion of 75 % of the small bowel.After intestinal exclusion an increase in acid secretion was found in the latter part of the acid response to the standard meal and the intestinal meal. No increase in acid secretion resulted from the meals which bypassed the small bowel.These findings suggest that an increase in stimulation from the remaining small intestine is responsible for the elevation in acid secretion following small bowel exclusion.An increase in gastric secretion following extensive small bowel resection or exclusion in dogs has been reported on many occasions since it was first described by Sabsai (1963). Yet the site of the abnormality in the gastric secretory mechanism has not been precisely localized.Theoretically, the increase in acid secretion could result from a change in vagal, antral, or intestinal stimulation of gastric secretion or from a change in the parietal cell response to these stimuli.Sabsai (1963) showed that an increase in the sham feeding response occurred after small bowel resection in dogs with vagally innervated pouches or gastric fistulae. Landor (1969), using dogs with Heidenhain pouches, demonstrated that an increase in gastric secretion could occur in the absence of the gastric antrum, indicating that the change in stimulation was arising, at least in part, from the small intestine.The purpose of this study was to determine the relative contributions of the vagus, the antrum, and the small intestine to the increase in acid secretion after small bowel exclusion. This was approached by measuring the acid responses alternately from stimulation of the stomach and the small intestine, with in each case the predominant exclusion of the other, before and after small bowel exclusion in dogs, some with vagally innervated pouches and some with vagally denervated pouches. Materials and MethodsThree adult mongrel dogs weighing 16-19 kg were prepared each with a vagally innervated fundic pouch (Gregory, Hallenbeck, and Code, 1942). The presence of vagal innervation to the pouches was confirmed by testing with intravenous insulin 0.4 u/kg, applying Hollander's criteria of incomplete denervation (Hollander, 1948). In addition, a permanent jejunal fistula was created 15 cm beyond the duodeno-jejunal flexure by means of a wide-bore titanium cannula of the Gregory pattern. A further four adult mongrel dogs, weighing 15-20 kg, were prepared with avagally denervated pouch and a jejunal fistula with a valve to prevent reflux of food introduced through the fistula (Figure 1 This consisted of 400 g of a commercial dog food (Banquet) composed of 11-5% protein, 7.5% fat, 1-5 % carbohydrate, 78.3 % wateIr, and 1-2 % mineral ash.

Effect of Jejunal Resection on the Gastric Acid Secretory Response to Pentagastrin, Histamine and Feeding in Dogs

“…However, 4 of their 5 dogs did increase their acid response. After small bowel exclusion, which also induces a postcibal gastric hypersecretion, an increase in the secretory response to histamine or pentagastrin has been observed in some experiments (24), but not in others (6). Our data indicate that after 50 % small bowel resection, there is an increase in the responses to histamine and pentagastrin from the Heidenhain pouch but not from the gastric fistula.…”

“…Thus, the hypothetical above-mentioned intestinal inhibitor could have both activities. Buxton et al (6), in an experiment utilizing small bowel exclusion, obtained secretory data which led them to suggest that increased acid secretion after small bowel exclusion might result from increased stimulation arising in the nonexcluded intestine. Yakimets and Bondar (36) have found a potent stimulant of gastric secretion in the thoracic lymph of enterectomizeddogs which is in agreement with Buxton's hypothesis.…”