Gastric hypersecretion produced by massive small bowel resection in dogs

Landor, John H.; Baker, Willis

doi:10.1016/s0022-4804(64)80023-8

Cited by 66 publications

(10 citation statements)

References 21 publications

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“…Studies in dogs with Heidenhain pouches have shown that an increase in gastric secretion can occur in the absence of vagal innervation of the gastric fundic mucosa (Sabsai, 1963;Landor and Baker, 1964;Frederick, Sizer, and Osborne, 1965;Westerheide, Elliot, and Hardacre, 1965;Reul and Ellison, 1966;Osborne, Frederick, Sizer, Blair, Cole, and Thum, 1966;Kerr, Elliott, and Endahl, 1968;Copeland, Miller, and Smith, 1968;Windsor, 1968;Landor, 1969;Santillana, Wise, Schuck, and Ballinger, 1969;Windsor, Fejfar, and Woodward, 1969;Burrington and Hamilton, 1969;Yakimets and Bondar;(1969) ;. Landor (1969) found that an increase in acid secretion followed small bowel resection in the absence of thegastricantrum in dogs with Heidenhain pouches.…”

Section: Discussionmentioning

confidence: 99%

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

Buxton¹,

Wasunna²,

Saunders³

et al. 1972

Gut

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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.

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Section: Discussionmentioning

confidence: 99%

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

Buxton¹,

Wasunna²,

Saunders³

et al. 1972

Gut

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“…Other workers have demonstrated hypersecretion of acid from Heidenhain pouches in dogs after massive intestinal resection (Landor and Baker, 1964;Westerheide, Elliott, and Hardacre, 1965;Reul and Ellison, 1966;Kerr, Elliott, and Endahl, 1968).…”

mentioning

confidence: 98%

Gastric secretion after massive small bowel resection

Windsor¹,

J²,

Woodward³

1969

Gut

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“…Massive small bowel resection is followed by gastric acid hypersecretion in man [5,15], dogs [12,18], and rats [3]. Since Straus et al [19] first observed hypergastrinemia in pa tients with short bowel syndrome, similar observations have been made in dogs [30] and rats [2], which suggest that gastrin may play a role in the gastric acid hypersecretion that is seen after extensive resections of the small intestine.…”

mentioning

confidence: 97%

Removal of Circulating Gastrin and Cholecystokinin into the Lumen of the Small Intestine

Inoue¹,

Ayalon²,

Yazigi³

et al. 1982

Digestion

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This study was undertaken to investigate the mechanism by which the small intestine removes circulating gastrin and cholecystokinin (CCK). A 100-cm (acute study, 10 dogs) or a 50-cm (chronic study, 5 dogs) segment of midjejunum was excluded in all 15 dogs. The excluded loop was perfused with 0.1 M phosphate buffer (pH 7.4), which was constantly recirculated by a peristaltic pump. In the acute control study (5 dogs), gastrin concentrations in the intestinal perfusate were increased gradually to a level of 320 ± 49 pg/ml at 90 min (i.e., 7.6 ± 0.9 times higher than serum gastrin levels). In the antrectomy group (5 dogs), perfusate gastrin concentrations were greatly decreased after antrectomy, in consonance with the decrease in serum gastrin concentrations. In the chronic study (5 dogs), perfusate gastrin concentrations were significantly increased after food stimulation, in consonance with the increase in serum gastrin concentrations. CCK was also released into the bowel lumen in considerable amounts basally and after endogenous release. Although one cannot exclude the possibility that a considerable amount of gastrin or CCK in the lumen may originate from the bowel segment, this study shows that the small bowel removes gastrin and CCK from the circulation by their secretion into the bowel lumen. Loss of this mechanism might partially explain the rise in gastrin levels that is observed in some patients after extensive small bowel resections.

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Gastric hypersecretion produced by massive small bowel resection in dogs

Cited by 66 publications

References 21 publications

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

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

Gastric secretion after massive small bowel resection

Removal of Circulating Gastrin and Cholecystokinin into the Lumen of the Small Intestine

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