Effect of enprostil on basal and meal-stimulated gastric acid and pepsin secretion, serum gastrin and gastric emptying in healthy persons

2007 ◽  
Vol 2 (1) ◽  
pp. 65-72 ◽  
Author(s):  
K. BERSTAD ◽  
H. MASSEY ◽  
A. BERSTAD
1983 ◽  
Vol 244 (5) ◽  
pp. G546-G551
Author(s):  
B. I. Hirschowitz ◽  
E. Molina

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.


1986 ◽  
Vol 31 (6) ◽  
pp. 561-566 ◽  
Author(s):  
H. P. M. Festen ◽  
H. A. R. E. Tuynman ◽  
J. D�fize ◽  
G. Pals ◽  
R. R. Frants ◽  
...  

1991 ◽  
Vol 261 (2) ◽  
pp. G295-G304 ◽  
Author(s):  
J. S. Redfern ◽  
H. J. Lin ◽  
K. E. McArthur ◽  
M. D. Prince ◽  
M. Feldman

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.


Gut ◽  
1983 ◽  
Vol 24 (1) ◽  
pp. 61-66 ◽  
Author(s):  
R Mohammed ◽  
R J Holden ◽  
J B Hearns ◽  
B M McKibben ◽  
K D Buchanan ◽  
...  

Gut ◽  
1979 ◽  
Vol 20 (5) ◽  
pp. 404-407 ◽  
Author(s):  
J A Forrest ◽  
M R Fettes ◽  
G P McLoughlin ◽  
R C Heading

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