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.

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.

Inhibition of gastric acid secretion by oxyntomodulin and its 19-37 fragment in the conscious rat

1993 ◽  
Vol 264 (5) ◽  
pp. G816-G823 ◽  
Author(s):  
C. Jarrousse ◽  
C. Carles-Bonnet ◽  
H. Niel ◽  
R. Sabatier ◽  
M. P. Audousset-Puech ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Gastric Fistula ◽  
Metabolic Clearance ◽  
Target Tissue ◽  
Dependent Manner ◽  
Conscious Rat ◽  
Basal Acid ◽  
Dose Dependent

Oxyntomodulin (Oxm) is a hormone, released from the intestine during digestion. Its target tissue is the gastric mucosa, where it inhibits acid secretion. It contains the 29-amino acid glucagon moiety, extended at its COOH-terminal end by an octapeptide. The glucagon moiety contains a basic doublet (Arg17-Arg18). Our working hypothesis was that the mode of action of Oxm may imply a processing of the molecule at the Arg-Arg doublet, releasing Oxm-(19-37). We compared the effect of Oxm with that of Oxm-(19-37) on gastric acid secretion in the conscious rat provided with a chronic gastric fistula. The acid secretion was plateau stimulated by a perfusion of either pentagastrin or histamine. Whereas Oxm or Oxm-(19-37) had no effect on basal acid secretion, both peptides inhibited pentagastrin (0.5 micrograms.kg-1.h-1)- and histamine (0.4 mg.kg-1.h-1)-stimulated acid secretion in a dose-dependent manner. When the metabolic clearance rate for each peptide was taken into account, the 19-37 fragment was as potent as the whole Oxm, regardless of the type of stimulant. When the dose of pentagastrin was increased from 0.175 to 1.1 micrograms.kg-1.h-1, the extent of inhibition induced by Oxm (40 pmol/kg) also increased. In contrast, when the dose of histamine was increased from 0.25 to 1.2 mg.kg-1.h-1, the extent of inhibition induced by Oxm (40 pmol/kg) decreased. Oxm-(19-37) (70-140 pmol/kg) displayed the same behavior as the whole molecule under both types of stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Cephalic phase of acid secretion involves activation of medullary TRH receptor subtype 1 in rats

2002 ◽  
Vol 283 (6) ◽  
pp. G1310-G1319 ◽  
Author(s):  
Vicente Martínez ◽  
María Dolores Barrachina ◽  
Gordon Ohning ◽  
Yvette Taché
Keyword(s):  
Acid Secretion ◽  
Serum Gastrin ◽  
Control Group ◽  
Receptor Subtype ◽  
Gastric Fistula ◽  
Sham Feeding ◽  
Cephalic Phase ◽  
Basal Acid ◽  
Fasted Rats ◽  
Trh Receptor

Mechanisms involved in the cephalic phase of gastric acid secretion were studied in awake fasted rats with chronic gastric fistula and exposed to the sight and smell of chow for 30 min. Acid secretion was monitored using constant intragastric perfusion and automatic titration. Sham feeding induced a peak acid response reaching 82 ± 7 μmol/10 min within 20 min compared with the average 22 ± 2 μmol/10 min in controls. The sham-feeding response was abolished by intracisternal pretreatment with the TRH1-receptor antisense oligodeoxynucleotides or subcutaneous injection of atropine, whereas TRH1 mismatch oligodeoxynucleotides had no effect. Serum gastrin was not altered by the sham feeding and increased by refeeding. Gastrin antibody did not block the rise in acid during sham feeding, although the net acid response was reduced by 47% compared with the control group. Glycine-gastrin antibody, indomethacin and nitro-l-arginine methyl ester had no effect. Atropine and gastrin antibody decreased basal acid secretion by 98 and 75%, respectively, whereas all other pretreatments did not. These results indicate that the cholinergic-dependent acid response to sham feeding is mediated by brain medullary TRH1 receptors in rats.

Evidence for reflex adrenergic inhibition of acid secretion in the conscious rat

1986 ◽  
Vol 251 (5) ◽  
pp. G615-G618 ◽  
Author(s):  
R. Dimaline ◽  
N. Carter ◽  
S. Barnes
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Chemical Stimulation ◽  
Gastric Distension ◽  
Gastric Fistula ◽  
Conscious Rat ◽  
Basal Acid ◽  
Stimulation Of

In conscious gastric fistula rats, gastric distension with saline to a pressure of 7 cm caused a threefold reduction of basal gastric acid secretion. Distension with 6.25% peptone solution to the same pressure doubled basal acid secretion. The saline distension-induced inhibition was abolished by guanethidine and markedly reduced by propranolol; phentolamine was ineffective. The response to peptone was unaffected by guanethidine. The results suggest that in the rat, gastric distension at physiological pressures inhibits acid secretion by a beta-adrenergic reflex. The inhibition can be masked by concurrent chemical stimulation of the gastric mucosa by the digestion products of food.

Effect of somatostatin on basal and stimulated gastric secretion in the cod, Gadus morhua

1988 ◽  
Vol 254 (2) ◽  
pp. G183-G188 ◽  
Author(s):  
B. Holstein ◽  
C. Cederberg
Keyword(s):  
Gastric Secretion ◽  
Acid Secretion ◽  
Gastric Acid ◽  
Gadus Morhua ◽  
Acid Output ◽  
Pepsin Secretion ◽  
Basal Acid Output ◽  
Basal Acid ◽  
Slight Inhibition

In vivo secretion of gastric acid and pepsin has been studied in pylorus-ligated cod. Basal acid output amounted to 100-150 mumol H+.kg-1.h-1 and pepsin secretion to 1 mg.kg-1.h-1. In response to bombesin nonapeptide (2.4 nmol.kg-1.h-1) and histamine (81 nmol.kg-1.h-1), acid secretion increased to approximately 200 and 600% of the basal level, respectively. Pepsin output was marginally affected by histamine but increased to approximately 3 and 15 times the basal level during treatment with bombesin and eledoisin (3.27 nmol.kg-1.h-1). Somatostatin (SS-14, 15 nmol.kg-1.h-1) inhibited basal acid secretion by 85%. It also inhibited the acid secretion during stimulation with bombesin (68%) and histamine (57%), but although the former effect could be explained by removal of the basal component, the latter could not. Basal pepsin secretion was not affected by SS-14. A slight inhibition (28%) of the peak pepsin response to eledoisin was demonstrated, and bombesin failed to stimulate pepsin secretion during treatment with SS-14. These results indicate that endogenous somatostatin, if present in the cod stomach, could play a role in the regulation of gastric secretion.

scholarly journals Effects of eight weeks' continuous treatment with oral ranitidine and cimetidine on gastric acid secretion, pepsin secretion, and fasting serum gastrin.

Gut ◽  
1983 ◽  
Vol 24 (1) ◽  
pp. 61-66 ◽  
Author(s):  
R Mohammed ◽  
R J Holden ◽  
J B Hearns ◽  
B M McKibben ◽  
K D Buchanan ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Serum Gastrin ◽  
Continuous Treatment ◽  
Pepsin Secretion ◽  
Fasting Serum
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