Characteristics of intestinal phase of gastric secretion

Abstract

In four dogs provided with special gastroduodenal fistulas allowing for the complete separation of stomach and duodenum without interrupting the vagal connections between them, the magnitude of the gastric and intestinal phases was compared and their contribution to the total gastric response to a meal was established. A liver extract (LE) meal, confined to the stomach and maintained at pH 5.0 by an intragastric titration technique, produced acid output reaching 66% of the maximal response to histamine (MRH). Perfusion of the LE meal into the duodenum resulted in acid secretion amounting to 57% of MRH. The combination of the gastric and intestinal phases caused the highest acid output, amounting to about 90% of MRH. Gastric and intestinal phases induced separately were accompanied by a significant elevation in serum gastrin concentrations which reached the highest values when both phases were evoked simultaneously. Acidification of the intestinal meal resulted in pH-dependent inhibition of gastric secretion falling to the basal values at pH 1.0. These secretory changes were mimicked by exogenous secretin. Serum gastrin levels remained essentially unaffected by the acidification of the intestinal meal while exogenous secretin significantly lowered them. In conclusion, in the intact stomach with undisturbed nervous connections between the stomach and duodenum, a peptone meal in the intestine is capable of evoking a potent gastric acid and pepsin stimulation by a mechanism involving the release of antral hormone.

Intestinal phase of gastric secretion in patients with duodenal ulcer

“…The mechanism of the potent intestinal stimulation of gastric secretion has been little studied in man and most of the information available has been derived from animal experiments (Buxton et al, 1972;Debas et al, 1975;Konturek et al, 1976). It has been suggested that the intestinal phase of stimulation of gastric acid and serum gastrin could be accounted for by the alleged release from the gut of two hormonal substances, entero-oxyntin (Debas et al, 1975), which directly stimulates the oxyntic glands, and enterobombesin, which stimulates the release of antral gastrin and gastric acid secretion (Erspamer and Melchiorri, 1975).…”

“…One of the criteria which was used in animals to distinguish the intestinal phase hormone (enterooxyntin) from non-specific stimulants such as antral type gastrin or cholecystokinin is the augmentation of the maximal response to pentagastrin or histamine (Debas et al, 1975;Konturek et al, 1976). It appears that this criterion can also be demonstrated in humans, particularly in duodenal ulcer patients, who show marked, prolonged, and highly significant augmentation of both gastric acid and pepsin responses to pentagastrin after a duodenal liver extract meal.…”

Inhibition of gastric secretion by fat and hypertonic glucose in the dog: role of gastric inhibitory peptide.

“…Numerous studies have demonstrated conclusively that intraduodenal administration of fat and concentrated glucose solutions inhibits gastric secretion (Konturek, Kaess, Kwiecien, Radecki, Dorner & Tackentrupp, 1976;. The possibility that duodenal inhibition of gastric secretion is a physiological phenomenon led to the search for specific hormones in extracts of duodenal mucosa which might be responsible for this inhibition (Johnson & Grossman, 1972).…”

“…This study has been undertaken to study the changes in plasma GIP levels in relation to the inhibition of post-prandial gastric acid secretion which occurs in response to fat and glucose administered into the stomach or duodenum in conscious dogs. METHODS Five dogs weighing between 18 and 24 kg were anaesthetized with thiobarbital sodium (25 mg/kg) and prepared with a gastroduodenal fistula drained by a large stainless steel cannula which has been described previously (Konturek et al 1976). A double-walled mucosal septum was constructed at the pylorus to separate the stomach from the duodenum.…”

“…The test meal consisted of a 5 % aqueous solution of liver extract (Reheis Chemical Co., Chicago) or saline (control) adjusted to pH 5-0 and administered continuously during 210-240 min. In tests on the gastric phase, 300 ml of the test meal were introduced into the stomach and acid output was determined by a modified intragastric titration technique described previously (Konturek et al 1976). The actual titration of gastric acid was performed in a titration chamber (volume 50 ml) that was attached to the hollow obturator of the gastroduodenal cannula.…”