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AJP - Gastrointestinal and Liver Physiology, Vol 241, Issue 5 403-G415, Copyright © 1981 by American Physiological Society
ARTICLES |
J. Miller, G. Kauffman, J. Elashoff, H. Ohashi, D. Carter and J. H. Meyer
Previous work has indicated that a chemoselective resistance controls gastric emptying. By use of meals of glucose or oleate, which were shown to empty spontaneously from dogs' stomachs half as fast as saline, we sought to locate this resistance by studying flow under controlled pressures in various regions of the gastrointestinal tract. In intact dogs, gastric outflow of glucose or oleate rose one-third as fast as outflow of saline as gastric pressure was raised, and this increased resistance to outflow of nutrients was unaffected by truncal vagotomy and pyloroplasty. In fistula dogs, gastroduodenal outflow rose linearly with gastroduodenal pressure gradients; outflow was markedly inhibited in a dose-related manner by intestinal oleate but not glucose. Inhibition by oleate was abolished by pyloroplasty. Glucose or oleate flowed into the small bowel from a barostat only slightly slower than saline. However, there was a strong inhibition of intestinal inflow of all three meals by gastric distension, an effect unaltered by truncal vagotomy. The findings suggest that gastric emptying is controlled by complex interactions among pressures and resistances, both within and beyond the stomach.
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