Failure of ?antigastrin? (SC-15 396) to inhibit gastric acid and pepsin secretion in anaesthetized gastric fistula cats

1968 ◽  
Vol 261 (1) ◽  
pp. 89-92 ◽  
Author(s):  
K. -Fr. Sewing ◽  
P. D. Gorinsky ◽  
F. Lembeck
Keyword(s):  
Gastric Acid ◽  
Gastric Fistula ◽  
Pepsin Secretion

Relation of gastric acid and pepsin secretion to serum gastrin levels in dogs given bombesin and gastrin-17

1983 ◽  
Vol 244 (5) ◽  
pp. G546-G551
Author(s):  
B. I. Hirschowitz ◽  
E. Molina
Keyword(s):  
Acid Secretion ◽  
Gastric Acid ◽  
Serum Gastrin ◽  
Gastric Fistula ◽  
Gastrin Release ◽  
Pepsin Secretion ◽  
Inhibitory Peptide ◽  
High Doses ◽  
Higher Doses ◽  
Stimulation Of

To quantitate bombesin stimulation of gastric acid and pepsin via release of gastrin, five gastric fistula dogs were given graded doses (60-1,250 pmol X kg-1 X h-1) of bombesin tetradecapeptide and 40-2,000 pmol X kg-1 X h-1 of synthetic gastrin-17 (G-17). Acid and pepsin output and serum gastrin were proportional to the dose of stimulant. The half-maximal dose of bombesin for gastrin release was 200 pmol X kg-1 X h-1. Bombesin-stimulated acid secretion related to serum gastrin concentrations was congruent with the G-17 curve, but with a maximum of only 62% of the G-17 maximum before declining by 27% despite higher serum gastrin levels. This suggested that bombesin stimulates acid secretion only via gastrin release and inhibits at higher doses by releasing another inhibitory peptide, most likely somatostatin, which is also released by bombesin. The same mechanism could apply to supramaximal inhibition of acid and pepsin seen with high doses of G-17. Because the pepsin curve related to serum gastrin was to the left of the G-17 curve, we concluded that another secretagogue released by bombesin acts synergistically with gastrin on pepsin secretion. Therefore, bombesin stimulates gastric secretion through gastrin release, but its effects are modified by peptides coreleased to a) increase pepsin output at low doses and b) limit the output of acid and pepsin to 50-60% of the G-17 maximum.

Gastric acid and pepsin hypersecretion in conscious rabbits

1991 ◽  
Vol 261 (2) ◽  
pp. G295-G304 ◽  
Author(s):  
J. S. Redfern ◽  
H. J. Lin ◽  
K. E. McArthur ◽  
M. D. Prince ◽  
M. Feldman
Keyword(s):  
Acid Secretion ◽  
Gastric Acid ◽  
Serum Gastrin ◽  
Gastric Fistula ◽  
Intragastric Ph ◽  
Pepsin Secretion ◽  
Cholinergic Pathways ◽  
Basal Serum ◽  
Maximal Output ◽  
Basal Acid

In conscious, gastric fistula rabbits, gastric acid and pepsin secretion averaged 4.5 +/- 0.1 mmol/h (1.3 mmol.kg-1.h-1) and 4.9 +/- 0.3 IU/h (1.6 IU.kg-1.h-1), respectively; these values represent approximately 40-50% of maximal output. Basal serum gastrin concentrations averaged 24 +/- 4 pg/ml and did not correlate with basal acid secretion. Atropine and vagotomy incompletely inhibited basal acid secretion (by 84 and 50%, respectively) and completely inhibited 2-deoxy-D-glucose-stimulated gastric acid secretion. Atropine and vagotomy similarly inhibited basal pepsin secretion by 50 and 40%, respectively. Ranitidine decreased acid and pepsin secretion, but as with atropine, inhibition was not complete (73 and 37%, respectively). Although omeprazole did not affect pepsin secretion, omeprazole completely inhibited basal acid secretion and elevated postprandial intragastric pH above 5.0. Conscious, gastric fistula rabbits have the highest basal acid and pepsin output among species commonly studied. Both vagal-cholinergic pathways and histamine drive basal acid and pepsin secretion in the rabbit.

Centrally administered NPY stimulated gastric acid and pepsin secretion by a vagally mediated mechanism

1991 ◽  
Vol 35 (1) ◽  
pp. 31-41 ◽  
Author(s):  
Masayuki Matsuda ◽  
Mitsuru Aono ◽  
Motoyuki Moriga ◽  
Minoru Okuma
Keyword(s):  
Gastric Acid ◽  
Pepsin Secretion

LATENCY OF THE GASTRIC SECRETORY RESPONSE TO SHAM FEEDING IN THE DOG

1967 ◽  
Vol 45 (4) ◽  
pp. 633-641 ◽  
Author(s):  
R. M. Preshaw
Keyword(s):  
Gastric Acid ◽  
Secretory Response ◽  
Conscious Dogs ◽  
Pepsin Secretion ◽  
Sham Feeding

In conscious dogs with gastric fistulas the latency of both the gastric acid and pepsin responses to sham feeding was about 6 min. When a background secretion was induced with various closes of hog gastrin, the latency of the acid response to sham feeding was unchanged, but the latency of the pepsin response was shortened. The peak rates of acid and pepsin secretion after sham feeding were not altered by the infusion of gastrin.

Effect of Secretin on Pentagastrin-Stimulated Gastric Acid and Pepsin Secretion after Vagotomy in Man

1973 ◽  
Vol 8 (2) ◽  
pp. 119-122
Author(s):  
A. Berstad ◽  
H. Petersen ◽  
M. Roland ◽  
I. Liavåg
Keyword(s):  
Gastric Acid ◽  
Pepsin Secretion

Inhibitory effects of beta-adrenergic agonists on gastric acid secretion in dogs

1986 ◽  
Vol 251 (4) ◽  
pp. G453-G459
Author(s):  
M. H. Stevens ◽  
R. C. Thirlby ◽  
C. T. Richardson ◽  
M. A. Fredrickson ◽  
R. H. Unger ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Intravenous Infusion ◽  
Acid Output ◽  
Gastric Fistula ◽  
Adrenergic Agonists ◽  
Inhibitory Effects ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonists

We evaluated the effect of two beta-adrenergic agonists, isoproterenol (nonselective agonist) and terbutaline (selective beta 2-agonist), on gastric acid secretion stimulated by intravenous pentagastrin, bethanechol, or histamine in dogs with gastric fistulas. Intravenous infusion of isoproterenol or terbutaline inhibited pentagastrin-stimulated acid secretion to a significantly greater extent than they inhibited bethanechol- or histamine-stimulated acid secretion. For example, isoproterenol (12 micrograms X kg-1 X h-1) reduced mean pentagastrin-, bethanechol-, and histamine-stimulated acid output by 86, 63, and 14%, respectively. Percent inhibition of acid secretion with terbutaline (30 micrograms X kg-1 X h-1) averaged 60, 17, and 24% for pentagastrin, bethanechol, and histamine, respectively. Terbutaline also inhibited pentagastrin-stimulated acid secretion from vagally denervated fundic pouches in a dose-related manner. Plasma somatostatin-like immunoreactivity was significantly higher during infusion of terbutaline plus pentagastrin than during infusion of pentagastrin alone. However, an intravenous infusion of 0.3 microgram X kg-1 X h-1 somatostatin-14 had no effect on pentagastrin-stimulated acid secretion from the gastric fistula, even though this infusion increased plasma somatostatin-like immunoreactivity to the same extent as terbutaline plus pentagastrin infusion. Thus the amount of somatostatin released during terbutaline infusion was not sufficient to explain the inhibition of pentagastrin-stimulated acid secretion observed.

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