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Gastric secretion after massive small bowel resection
This paper confirms that gastric hypersecretion can occur in man and dogs after massive intestinal resection. The assumption, made by others, that hypersecretion in the clinical situation is similar to that observed in dogs is challenged. An acute hypersecretory state occurred in eight of 19 patients after massive intestinal resection. This was apparent as an increased rate of basal secretion. It was usually transient and unrelated to the length of intestine resected. A correlation was noticed between hypersecretion and jaundice in the immediate postoperative period. Histamine release after acute hepatic injury was postulated as the cause of the hypersecretion. By contrast a chronic gastric hypersecretory state was demonstrated in dogs after massive intestinal resection. The rate of basal secretion was not significantly altered. The increased daily acid output was shown to be due to prolonged and enhanced response to food. The cause was thought to be loss of inhibitory agents, such as enterogastrone, normally released by the small intestine when in contact with food. The rationale of performing vagotomy and pyloroplasty at the same time as the intestinal resection is questioned.
This paper confirms that gastric hypersecretion can occur in man and dogs after massive intestinal resection. The assumption, made by others, that hypersecretion in the clinical situation is similar to that observed in dogs is challenged. An acute hypersecretory state occurred in eight of 19 patients after massive intestinal resection. This was apparent as an increased rate of basal secretion. It was usually transient and unrelated to the length of intestine resected. A correlation was noticed between hypersecretion and jaundice in the immediate postoperative period. Histamine release after acute hepatic injury was postulated as the cause of the hypersecretion. By contrast a chronic gastric hypersecretory state was demonstrated in dogs after massive intestinal resection. The rate of basal secretion was not significantly altered. The increased daily acid output was shown to be due to prolonged and enhanced response to food. The cause was thought to be loss of inhibitory agents, such as enterogastrone, normally released by the small intestine when in contact with food. The rationale of performing vagotomy and pyloroplasty at the same time as the intestinal resection is questioned.
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