In 3 cats with gastric fistulas, Heidenhain pouches, and duodenal cannulas, instillation of 15 ml of emulsified fat into the duodenum stimulated acid secretion from the Heidenhain pouches. Pentagastrin (1, 2, 4, and 8 μg per kg-hr) or histamine dihydrochloride (0.02; 0.04, 0.08, and 0.16 μg per kg-hr) were given by intravenous infusion and acid output was measured from the Heidenhain pouches with the gastric fistulas open. Either 15 ml of fat or 0.15 M NaCl solution was infused into the duodenum after acid secretion had reached a plateau. Fat increased acid secretion from the Heidenhain pouches at all doses of pentagastrin or histamine; the increase was greatest at low doses and became insignificant at higher doses. Intravenous infusion of 8.0 U per kg-hr of cholecystokinin evoked acid secretion which was slightly less than that induced by 15 ml of fat in the duodenum. When this dose of cholecystokinin was given with varying doses of pentagastrin, acid secretion increased at the lower pentagastrin doses but not at the higher ones. Therefore, in cats, both fat in the intestine and exogenous cholecystokinin behave as full agonists for acid secretion. There is no evidence that fat releases any substance in this species which could be considered an enterogastrone.
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