Effect of vagotomy on gastric acid secretion in the rat

The effects of pentagastrin, histamine or feeding on gastric acid secretion were studied in conscious rats with total gastric by-pass, achieved by transection of the cardia and pylorus, followed by an oesophago-duodenostomy. After closure of the cardia, the by-passed stomach was connected to the small intestine through a Roux-en-Y loop. A chronic gastric fistula was fitted into the rumen. Basal acid output was low in chronically vagotomized rats, being 6% of that in the innervated animals. A clear-cut stimulation was observed after both pentagastrin and histamine in innervated as well as denervated rats, although the maximal acid output in the denervated group was less than 10% of that in the innervated group. In previous studies on acid secretion in vagotomized rats with chronic gastric fistulas, neither basal nor stimulated acid secretion could be detected. Apparently, by-passing the stomach eliminates sources of error associated with the conventional gastric fistula technique (for instance, neutralization of acid gastric juice by swallowed saliva or regurgitated duodenal juice). Nonetheless, the greatly reduced acid output following vagotomy indicates that normal basal as well as normal stimulated acid secretion is dependent upon an intact vagus. Pentagastrin- and histamine-stimulated acid secretion was blocked by atropine and cimetidine in both the innervated and denervated rats. Feeding caused a significant inhibition of acid secretion in the by-passed, innervated stomach. In the denervated stomach feeding was without effect. The mechanism behind the postprandial inhibition of acid secretion in the innervated stomach is obscure. Direct vagal inhibition as well as humoral substances, liberated by vagal stimulation or by the presence of food in the intestine, may be responsible.