Search PubMed⌕ Search

Biomedical subjects

D F Magee

Publications and source records attributed to D F Magee.

At least 55 records · Page 3Linked to original sources
PubMed1978

Do beta adrenergic agents directly stimulate gastrin secretion?

Isoproterenol if given during methacholine stimulation in dogs neither depresses gastric secretion nor elevates serum gastrin. Therefore, we conclude that beta adrenergics (isoproterenol) are unlikely to be direct liberators of gastrin, but raise serum gastrin indirectly only if they inhibit gastric secretion.

Animals↗
PubMed1977

Modification of the action of pentagastrin on acid secretion by botulinum toxin.

I.v botulinum toxin after 60-90 min abolished the dose-response relationship between pentagastrin and gastric acid secretion in anesthetized rats and guinea-pigs. The toxin reduced but did not abolish the acid stimulatory effect of histamine. As expected, the acid response to vagal stimulation was abolished and that to methacholine in rats was unaltered by the toxin.

Acetylcholine↗
PubMed1977

The secretion of pepsin.

1. Ligation and division of the vessels supplying the stomach, except those from the spleen, result in greatly increased pepsin secretion in response to pentagastrin, pilocarpine or 2-deoxy-D-glucose. 2. This effect was still present 6 months after initial ligation. 3. Analysis of dose-response curves shows that for pepsin secretion the Vmax values were raised by this procedure. 4. Right-sided vessel ligation and division does not alter acid secretion in response to the stimuli used. 5. It is suspected that the procedure of right-sided vessel ligation removes a non-competitive inhibitor mechanism to gastric pepsin secretion.

Animals↗
PubMed1977

Evidence for antral inhibition of pentagastrin from experiments using mucosal cooling.

1. The acid secretion of the fundic mucosa in Heidenhain pouches in response to pentagastrin became progressively less as the pouch mucosa was cooled. 2. When a cooled Heidenhain pouch in an animal receiving pentagastrin was warmed, acid and pepsin secretion from the main stomach was depressed. Change from warm to cool produced no obvious effect. 3. In animals receiving pentagastrin continuously, but not in those receiving histamine, lowering the temperature in an antral pouch, or the application of local anaesthetics to its mucosa, increased acid and pepsin secretion from the main stomach when the antral pouch was fully innervated. 4. This effect could readily be abolished by ganglionic and beta-adrenergic blockade, but not by bilateral vagal block in the neck, thus suggesting a sympathetically mediated inhibitory mechanism of pyloric origin. 5. The effect of indirect vagal stimulation, using 2-deoxy-D-glucose on secretion from the main stomach, was augmented by pyloric antral local anaesthesia and depressed by antral cooling.

Animals↗
PubMed1976

Adrenergic activity and gastric secretion.

Isoproterenol infusions depress pentagastrin (PG)-stimulated secretion of acid and pepsin from both gastric fistulae and denervated (Heidenhain) pouches in conscious dogs. It was not found to do so if methacholine replaced gastrin. Propranolol reversed the isoproterenol depression of PG stimulation but had no effect on isoproterenol plus methacholine except on the fistula where both acid and pepsin were depressed. It is felt that PG and methacholine act by differing mechanisms both on chief and parietal cells.

Animals↗
PubMed1975

Heidenhain pouch distension as a stimulus for acid and pepsin secretion.

Heidenhain pouches, in dogs with simple gastric fistulae, were distended with saline (30, 60 and 90 ml). Pouch acid and pepsin increased linearly with increasing saline volume. Additional pentagastrin augmented the acid but antagonized the pepsin responses. Atropine depressed both the acid and pepsin responses to distention. Ganglionic blockade and local anesthetization of the secretory mucosa also depressed the acid but spared the pepsin response.

Animals↗
PubMed1975

Metiamide: an antagonist of histamine-stimulated gastric acid secretion.

Metiamide, 25 mg, antagonized the action of histamine on acid and pepsin secretion from both denervated pouches and innervated stomachs in dogs. In the same preparations its action on pepsin following food, pentagastrin or 2 deoxy-d-glucose was nonsignificant. Following pilocarpine or secretin, metiamide augmented pouch pepsin. The action of every acid stimulant was depressed by metiamide including the direct vagal action of deoxy-d-glucose on the innervated stomach. H2 receptors seem, therefore, to be involved in some form in acid stimulated by the vagi, histamine, pentagastrin and pilocarpine. Pepsin stimulation does not seem to be via H2 receptors with the esception of stimulation by histamine itself.

Animals↗
PubMed1975

Action of morphine sulfphate on stimulated gastric secretion in dogs.

In dogs morphine sulphate suppresses both 2-deoxy-D-glucose and pentagastrin-stimulated acid and pepsin secretion, but not histimaine- and pilocarpine-stimulated acid. This is consistent with the view that morphine both depresses acetylcholine release from cholinergic endings in the stomach and that pentagastrin acts by liberation of acetylcholine from these endings.

Acetylcholine↗
PubMed1974

Pepsin.

Explore the source record for details and available documents.

Acetylcholine↗
PubMed1974

Inhibition of Heidenhain pouch pepsin secretion by commercial cholecystokinin and duodenal fat in dogs.

In unanesthetized dogs with Heidenhain pouches and separated duodenal pouches, intravenous infusion of commercial cholecystokinin (1.0 IDU per min) produced a significant depression of pouch acid and pepsin secretion stimulated by pentagastrin (1.0 microg per min) or by methacholine (2.0 microg per min). Acid response to methacholine was temporarily augmented. Irrigation of the duodenal pouches with emulsified fat produced similar patterns of depression of acid secretion in response to pentagastrin and pepsin secretion in response to pentagastrin or methacholine. Acid secretion stimulated by methacholine was temporarily augmented after the irrigation. It is concluded that fat releases endogenous cholecystokinin from the duodenal mucosa and that cholecystokinin, or duodenal fat, powerfully depresses Heidenhain pouch pepsin secretion in dogs. The involvment of the gastric inhibitory polypeptide (GIP) cannot be assessed from the present experiments.

Animals↗