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D F Magee

Publications and source records attributed to D F Magee.

At least 37 records · Page 2Linked to original sources

Comparison of the action of cholinomimetics and pentagastrin on gastric secretion in dogs.

Stimulation of acid secretion by muscarinic cholinomimetic agents depended on the periodic interdigestive activity of the stomach. This explains the peak and following fade. Pentagastrin stimulated gastric secretion after a fixed interval and did not depend on the interdigestive activity. Neither gastrin nor methacholine directly contracted the gallbladder in the doses used. A sustained secretion of gastric acid and pepsin, such as follows a meal, required both hormonal stimulation and gastric distension. The magnitude of the acid response from Heidenhain pouches following meals suggested that pentagastrin doses commonly used experimentally greatly exceed the physiological.

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Vagal control of gall-bladder contraction.

The role of the vagi in gall-bladder contraction was studied in conscious dogs with chronic biliary fistulae. The interdigestive periodic contraction of this organ was abolished by bilateral cervical vagal blockade, atropine or pentolinium, but neither methacholine nor carbachol initiated contraction when the duodenum was kept alkaline. The orthodox view that gall-bladder evacuation is primarily controlled by humoral mechanisms needs re-evaluation. Vagal blockade prevented the usual gall-bladder contraction in response to duodenal acidification.

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The role of motilin in periodic interdigestive pancreatic secretion in dogs.

The role of motilin in the periodic interdigestive secretion of the pancreas was studied in conscious dogs, each with a chronic gastric fistula, a Heidenhain pouch and a Thomas duodenal fistula. Motilin increased pancreatic water, bicarbonate and protein secretion and the motility of the stomach, duodenum and Heidenhain pouch in a manner which closely resembles the spontaneous changes which occur during interdigestive activity. Endogenous motilin released by duodenal alkalinization had the same effect as exogenous hormone. Continuous infusion of motilin did not cause continuous pancreatic secretion and gut motility but merely shortened the interval of the periodic interdigestive activity. Exogenous and endogenous motilin were ineffective following atropine. Hexamethonium abolished the pancreatic and duodenal peaks but not the changes in gastric and pouch motility induced by motilin or duodenal alkalinization.

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Biphasic action of intravenous ethanol on dog exocrine pancreatic secretion.

The effect of a 20-min intravenous infusion of 1 g/kg of ethanol on a 15% (w/w) solution in isotonic saline on pancreatic secretion was determined in six conscious Beagle dogs provided with Thomas cannulae. Ethanol was given on a background of a prolonged infusion of 0.5 CU/kg/hr of secretin alone or secretin plus either different doses of cerulein (12.5-200 ng/kg/hr), 3 micrograms/kg/hr of pentagastrin, or 200 micrograms/kg/hr bethanechol. Intravenous ethanol had a biphasic action on pancreatic secretion: inhibition during the first 40 min followed by stimulation. When compared to control experiments with intravenous infusion of saline, the inhibition was statistically significant only for volume and bicarbonate output against a background of pentagastrin and for protein output against a background of bethanechol. We propose that alcohol inhibits acetylcholine-mediated protein secretion. The delayed stimulatory effect of ethanol was statistically significant for both ecobolic (protein output) and hydralatic (water and bicarbonate) secretion during infusion of secretin plus 12.5-25 ng/kg/hr cerulein, but not with doses of 50 ng/kg/hr. Although the plateau of secretion before alcohol was roughly similar in the experiments using cerulein and bethanechol, ethanol inhibited protein output and had no effect on bicarbonate output during stimulation with bethanechol. Therefore, the effects of alcohol on pancreatic secretion are influenced by both the type of stimulation and its intensity (dosage).

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The role of nicotinic receptors in dog pancreatic exocrine secretion.

1 The effects of pentamethonium, an autonomic ganglion blocker, were studied on the exocrine pancreatic secretion of six conscious dogs given intravenous infusions of urecholine, caerulein or pentagastrin on a background of submaximal doses of secretin. 2 Urecholine-induced protein secretion was not affected but both caerulein- and to a smaller extent, pentagastrin-induced protein secretions were depressed by pentamethonium. 3 These results indicate that intravenous caerulein and pentagastrin, but not urecholine, act at least partially via nicotinic receptors. 4 Volume and bicarbonate output were depressed by pentamethonium when stimulated by intravenous caerulein with a background of secretin, but not when stimulated by pentagastrin on a background of secretin. 5 From these data it is suggested that caerulein and pentagastrin may potentiate secretin-stimulated hydrelatic secretion by different mechanisms.

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Cyclic changes of plasma pancreatic polypeptide and pancreatic secretion in fasting dogs.

Fasting conscious dogs, each with a gastric fistula, Heidenhain pouch and Thomas duodenal fistula, were used. Basal pancreatic secretion showed periodic increases in phase with the periodic contraction of the stomach and duodenum. Periodic increases of plasma pancreatic polypeptide (PP), but not of gastrin, were observed in phase with the periodic contraction and secretion of the gut. Ganglion blockade abolished the cyclical activity, both secretory and motor, of the gut and of plasma PP. Intraduodenal infusion of lidocaine suppressed the spontaneous increase of pancreatic secretion and plasma PP. It is concluded both that the cyclical release of PP and the increase in pancreatic secretion are under the control of the intrinsic nerves of the duodenum.

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Neural control of periodic secretion of the pancreas and the stomach in fasting dogs.

The role of nerves in periodic secretion of the pancreas and the stomach in relation to the motility of the upper gastrointestinal tract was studied in conscious fasting dogs which had previously been provided with chronic gastric and pancreatic fistulae and a Heidenhain pouch. Both atropine and pentolinium abolished the periodic increase in gastric and pancreatic secretion and motility of the gut. Bilateral cervical vagal blockade with lidocaine reduced the motility of the stomach, the duodenum and the pouch preceding their peaks, but the motility at the peaks remained unchanged except in the case of the stomach. Pancreatic secretion preceding its peak was also decreased by vagal blockade but that at the peak was not significantly different from the control peak. Periodic pepsin secretion, from both the fistula and pouch, was decreased by vagal blockade. It is concluded that the secretion and motility of the upper gut in fasting dogs is controlled by periodic activity of the vagus and intrinsic nerves.

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Exogenously stimulated gastric secretion in dogs after ganglion and sympathetic blockade and antral acidification.

1 In conscious dogs with gastric fistulae, Heidenhain pouches and in some cases, innervated pyloric pouches, ganglionic blockade augmented Heidenhain pouch acid secretion only if the gastric fistula remained closed in animals receiving pentagastrin. 2 Ganglionic blockade depressed methacholine-stimulated acid and pepsin secretion from the Heidenhain pouch whether or not the fistula was open. 3 Acidification of the antral pouch consistently augmented the acid and pepsin secretion from the Heidenhain pouch when either pentagastrin or methacholine was the stimulus. Ganglionic blockade prevented this.

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The role of gastric secretion in post-diverted pancreatic hypersecretion in conscious rats.

1. In rats prepared with chronic external pancreatic fistulae, gastric fistulae and choledocho-enterostomy, the volume and protein secretion of pancreatic juice was measured. 2. The pancreatic secretion of water and protein after juice diversion was significantly lower when the gastric fistula was open than when closed. Secretion was abolished after atropine, with the fistula open and in animals with ligated pylori. 3. Intraduodenal HCl significantly raised juice volume and protein in animals with diverted juice when the gastric fistula was open. 4. Soybean trypsin inhibitor produced a significantly smaller elevation of juice volume and protein when the gastric fistula was open. 5. It is concluded that the initial hypersecretion of pancreatic juice and protein, following its diversion from the duodenum, is a consequence of the entry of gastric juice into the intestine.

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Effect of pancreatic juice on basal pancreatic and gastric secretion in dogs.

1. The effect of duodenal infusion of pancreatic juice on basal pancreatic and gastric secretion was studied in five conscious dogs provided with pancreatic fistulae, gastric fistulae and Heidenhain fundic pouches. 2. Pancreatic juice and trypsin stimulated a pancreatic secretion rich in protein. 3. Autodigested juice without proteolytic activities also stimulated the secretion. Boiling the juice or addition of trypsin inhibitor to the juice diminished the augmented secretion. 4. It seems, therefore, that trypsin is necessary even in proteolytically inactive autodigested juice for pancreatic stimulation. 5. In dogs, unlike rats and pigs, basal pancreatic secretion is not under negative feed-back control by duodenal tryptic activity. 6. Basal gastric secretion was not significantly changed by duodenal infusion of pancreatic juice.

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A study of gastric secretion in dogs using pilocarpine.

1 Pilocarpine (40 microgram/min i.v.) stimulated acid and pepsin secretion from Heidenhain pouches but did not stimulate secretion from the innervated stomach. 2 Pilocarpine significantly increased acid secretion from the innervated main stomach after the vagal nerves were bilaterally blocked with lidocaine. 3 The effect of pilocarpine on secretion from the Heidenhain puch was depressed by ganglionic blockade (hexamethonium), by dopamine and by isoprenaline. 4 The stimulatory action of histamine on gastric secretion from either pouch or gastric fistulae was uninfluenced by dopamine. 5 The action of pilocarpine was augmented by the muscarinic ganglionic stimulant AHR 602. Considering this effect, as well as the secretory depression of isoprenaline, pilocarpine resembles pentagastrin rather than methacholine in its action.

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