Vagotomy confined to the acid-secreting mucosa of the stomach

1987 ◽  
Vol 73 (1) ◽  
pp. 25-30
Author(s):  
E. P. Dewar ◽  
N. S. Williams ◽  
M. F. Dixon ◽  
D. Johnston
Keyword(s):  
Gastric Secretion ◽  
Myenteric Plexus ◽  
Acid Output ◽  
Gastric Wall ◽  
Neural Tissue ◽  
Gastric Fistula ◽  
Gastric Acid Output ◽  
Before And After ◽  
Acid Secreting ◽  
Gastric Musculature

AbstractChemoneurolysis, using varying concentrations of ethyl alcohol, was performed in dogs with a total gastric fistula in an attempt to denervate selectively only the acid-secreting mucosa, leaving the muscle innervated. Tests of gastric secretion and histological examination of gastric wall biopsies were performed both before and after chemoneurolysis. Chemoneurolysis resulted in a significant reduction in the number of parasympathetic fibres in the submucosa (p<0.01) and a decrease in insulin and pentagastrin stimulated acid secretion. The appearances of the myenteric plexus and gastric musculature were unchanged. The destruction of the submucosal neural tissue was, however, insufficient to produce a th erapeutically significant decrease in gastric acid output.

Neurotensin and oxyntomodulin-(30-37) potentiate PYY regulation of gastric acid and somatostatin secretions

1993 ◽  
Vol 265 (1) ◽  
pp. G113-G117 ◽  
Author(s):  
A. Bado ◽  
D. Cloarec ◽  
L. Moizo ◽  
J. P. Laigneau ◽  
D. Bataille ◽  
...  
Keyword(s):  
Gastric Acid ◽  
Intravenous Infusion ◽  
Peptide Yy ◽  
Acid Output ◽  
The Other ◽  
Gastric Fistula ◽  
Gastric Acid Output ◽  
Heidenhain Pouch ◽  
Basal Acid ◽  
Gastric Secretions

The present study was designed to investigate, in cats provided with both a gastric fistula and a denervated fundic Heidenhain pouch, the effect of peptide YY (PYY) on pentagastrin-stimulated gastric acid and somatostatin secretions and to determine whether neurotensin (NT) and the COOH-terminal octapeptide of oxyntomodulin [Oxm-(30-37)] would modify these secretions. Intravenous infusion of PYY (0.1 nmol.kg-1.h-1), NT (15 nmol.kg-1.h-1), or Oxm-(30-37) (60 nmol.kg-1.h-1) did not affect basal acid secretion. However, they significantly inhibited pentagastrin-stimulated gastric acid output up to 50% (P < 0.01) in the main stomach. Furthermore, they significantly increased gastric somatostatin release by +750, +1,700, and +600% over basal level (P < 0.01) for (in nmol.kg-1.h-1) 0.1 PYY, 15 NT, and 60 Oxm-(30-37), respectively. On the other hand, the effects of 0.1 nmol.kg-1.h-1 PYY were potentiated by subthreshold doses of NT (5 nmol.kg-1.h-1) or Oxm-(30-37) (15 nmol.kg-1.h-1). These findings suggest that there could be a cooperation between the three peptides in the intestinal regulation of gastric secretions.

Pharmacological evidence for histamine H3 receptor in the control of gastric acid secretion in cats

1991 ◽  
Vol 260 (4) ◽  
pp. G631-G635 ◽  
Author(s):  
A. Bado ◽  
F. Hervatin ◽  
M. J. Lewin
Keyword(s):  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Gastric Fistula ◽  
Gastric Acid Output ◽  
H2 Receptor Antagonist ◽  
H2 Receptor ◽  
H3 Receptor

We investigated the possible involvement of H3 receptor in the control of gastric acid secretion in the conscious cat provided with a gastric fistula [main stomach (MS)] and a denervated Heidenhain pouch (HP). Intravenous infusion of the selective H3 agonist (R)-alpha-methylhistamine at 3, 10, and 30 nmol.kg-1.h-1 induced a dose-related inhibition of pentagastrin-stimulated gastric acid output. Maximal inhibition in MS (48 +/- 3%, P less than 0.01) and HP (36 +/- 5%, P less than 0.01) was obtained with 30 nmol.kg-1.h-1. This dose also significantly inhibited peptone meal-induced gastric acid output by 38 +/- 4 and 46 +/- 8% (P less than 0.01) in MS and HP, respectively. These inhibitions were completely prevented by 10 nmol.kg-1.h-1 iv of the selective H3 receptor antagonist thioperamide. On the other hand, (R)-alpha-methylhistamine was without any effect on histamine-stimulated gastric acid output, whereas thioperamide produced a slight but not significant increase of this output in contrast to the H2 receptor antagonist ranitidine, which showed a strong inhibitory effect. These findings suggest that pentagastrin- or meal-induced gastric acid secretion involves an H3 receptor pharmacologically distinct from the H2 receptor.

Effects of Helicobacter pylorigastritis on gastric secretion in healthy human beings

1998 ◽  
Vol 274 (6) ◽  
pp. G1011-G1017 ◽  
Author(s):  
Mark Feldman ◽  
Byron Cryer ◽  
Edward Lee
Keyword(s):  
Gastric Secretion ◽  
Gastric Acidity ◽  
Serum Gastrin ◽  
Acid Output ◽  
Human Beings ◽  
Healthy Human ◽  
Women Subjects ◽  
Before And After ◽  
H Pylori ◽  
Antibody Levels

Helicobacter pylori gastritis is common, but effects on gastric secretion are not well understood. We measured basal and pentagastrin-stimulated gastric acidity, pepsin activity, and fluid output, as well as serum gastrin concentrations and H. pylori antibody levels, before and after treatment of H. pylori gastritis in 28 men and women. Subjects were studied before and 1 and 3 mo after a course of bismuth, metronidazole, and tetracycline. Elimination of H. pylori gastritis, accomplished in 14 subjects, increased basal and pentagastrin-stimulated gastric acidity (by 15 meq/l) and basal acid output significantly (by 2.1 meq/h 1 mo after therapy). Elimination of H. pylori had an opposite effect on pepsin secretion, significantly decreasing pepsin output by 30%. Elimination of H. pylori significantly reduced nonparietal fluid output by 35%, without affecting fluid output from parietal cells. Serum gastrin and H. pylori antibody levels declined significantly after elimination of H. pylori. None of these changes was observed in 14 subjects whose H. pylori gastritis was resistant to antimicrobial therapy. In summary, eradication of H. pylori infection increases gastric acidity by reducing nonparietal gastric secretion from peptic and other cells.

Effect of total adrenalectomy on gastric secretion in chronic gastric fistula rats

1964 ◽  
Vol 206 (6) ◽  
pp. 1309-1314 ◽  
Author(s):  
S. P. Bralow ◽  
S. A. Komarov ◽  
H. Shay
Keyword(s):  
Gastric Secretion ◽  
Parietal Cell ◽  
Free Acid ◽  
Acid Output ◽  
Cell Mass ◽  
Chloride Concentration ◽  
Sham Operation ◽  
Gastric Fistula ◽  
Total Acid ◽  
Total Chloride

Basal gastric secretion of rats with chronic fistulas was studied before and after adrenalectomy or sham operation. A marked exponential fall in concentration and output of free and total acid resulted in virtual anacidity within 3–7 weeks following adrenalectomy. Failure in parietal cell secretion was not accompanied by significant decrease in parietal cell mass. Pepsin concentration and output as well as volume also fell exponentially but more gradually. No significant change in total chloride concentration occurred. Relative influence of concentration in determining output was 30 times greater than volume for free acid, 3 times greater for total acid, and twice as great for pepsin. Volume was responsible for almost all variability in total chloride output. Time after adrenalectomy influenced variability of volume and acid output twice as much as concurrent decrease in body weight.

Effect of Atropine on Histamine-Stimulated Gastric Secretion in the Dog

1956 ◽  
Vol 186 (3) ◽  
pp. 373-376 ◽  
Author(s):  
Henry D. Janowitz ◽  
Franklin Hollander
Keyword(s):  
Gastric Secretion ◽  
Parietal Cell ◽  
Acid Output ◽  
Inhibitory Effect ◽  
Atropine Sulphate ◽  
Secreting Cell ◽  
Secretory Rate ◽  
Acid Secreting ◽  
The Mean

Inhibitory effect of atropine on gastric acid secretion was studied in four dogs with vagally denervated corpus pouches, stimulated by 0.025 mg of histamine-base subcutaneous every 10 minutes. The mean inhibition of acid output in the 3rd hour after subcutaneous injection of atropine sulphate was 29% at 0.1 mg/kg body weight, 31% at 0.2 mg/kg, and 96% at 0.4 mg/kg. At the highest dosage, inhibition was virtually complete in six of seven experiments. Since current concepts of cholinergic blocking action by atropine on gastric secretion are not completely explanatory of the present results, possible alternative formulations of the role of acetylcholine and histamine in stimulating the parietal cell are presented. One of these postulates that histamine is the final common chemical pathway for all stimuli to the acid secreting cell. The existing evidence for this is reviewed briefly. In addition, further striking evidence is presented to support the hypothesis that the primary (parietal cell) acidity is relatively constant and independent of the secretory rate.

Mechanism of action of insulin hypoglycemia on gastric secretion in man

1960 ◽  
Vol 15 (4) ◽  
pp. 697-703 ◽  
Author(s):  
David C. H. Sun ◽  
Harry Shay
Keyword(s):  
Gastric Secretion ◽  
Mechanism Of Action ◽  
Adrenal Glands ◽  
Acid Output ◽  
Late Phase ◽  
Inhibitory Effect ◽  
Maximal Response ◽  
Insulin Hypoglycemia ◽  
Before And After ◽  
Total Adrenalectomy

The effect of insulin hypoglycemia on acid output of gastric secretion over 5-hour periods was studied in eighteen patients with duodenal ulcer, five patients before and after vagotomy and two patients before and after bilateral total adrenalectomy. Results of this study show three components of the mechanism of action of insulin hypoglycemia on gastric secretion, an initial inhibitory effect on basal gastric secretion, a stimulating effect mediated through the vagus nerve responsible for the early phase of secretion (1st and 2nd hr.) and. a gastric secretory response mediated through the adrenal glands manifested in the late phase of secretion (3rd–5th hr.). However, the magnitude of this late phase of gastric secretion was considerably less pronounced after vagotomy. It appears that a maximal response of this phase of gastric secretion following insulin hypoglycemia dependent on the adrenal gland is also dependent upon an intact vagal mechanism. A significant hypoglycemia of 40 mg % or less was necessary to produce the late phase of gastric secretion. The adrenal phase can contribute to the potential for ulcer occurrence or reactivation, not so much through the increase in secretion it alone might induce, since this is small, but of greater importance in its synergistic action with the vagal mechanism. Submitted on December 9, 1959

Inhibition of bombesin-stimulated acid secretion by immunoneutralization of gastrin in dogs

1995 ◽  
Vol 268 (1) ◽  
pp. G54-G58
Author(s):  
T. O. Kovacs ◽  
K. C. Lloyd ◽  
H. Wong ◽  
J. H. Walsh
Keyword(s):  
Monoclonal Antibody ◽  
Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Gastric Fistula ◽  
Gastrin Release ◽  
Gastric Acid Output ◽  
Plasma Gastrin

Bombesin-like peptides stimulate gastrin release and gastric acid secretion. The increase in gastric acid output is thought to be secondary to gastrin release. A monoclonal antibody (MAb) directed specifically to gastrin (MAb 28.2) was used to study the role of circulating gastrin in the regulation of bombesin-stimulated acid secretion in dogs. Seven conscious, fasted dogs with gastric fistulas received intravenous bombesin infusions in fourfold increasing doses from 200 to 3,200 pmol.kg-1.h-1. Each dose was given for 45 min. On separate days, dogs were pretreated with an intravenous infusion of 7 mg of MAb 28.2 or vehicle (0.1% canine serum albumin). Samples of gastric effluent were collected by gravity drainage through the gastric fistula, and acid output was measured by titration of gastric effluent to pH 7.0, using 0.2 N NaOH. Plasma gastrin concentrations were determined by radioimmunoassay. Bombesin infusion produced dose-dependent increases in plasma gastrin concentrations and gastric acid output. Administration of gastrin MAb 28.2 abolished bombesin-stimulated gastric acid output. Immunoneutralization of circulating gastrin in vivo using a gastrin monoclonal antibody in dogs indicates that the acid stimulatory response to bombesin is mediated by gastrin.

Effects of KCl and insulin on benzimidazole-inhibited canine gastric secretion

1983 ◽  
Vol 245 (6) ◽  
pp. G739-G744
Author(s):  
B. I. Hirschowitz ◽  
J. Fong
Keyword(s):  
Gastric Secretion ◽  
Parietal Cell ◽  
Acid Output ◽  
Gastric Fistula ◽  
Large Decrease ◽  
Pepsin Secretion ◽  
K Secretion ◽  
Inhibited Acid ◽  
K Concentration ◽  
Bethanechol Chloride

The final step in acid secretion is believed to result from the H+-K+-ATPase-mediated exchange of H+ in the parietal cell, with K+ in the lumen. To study the K+ secretion we used Picoprazole and insulin separately and together to inhibit gastric secretion stimulated in gastric fistula dogs with histamine (100 micrograms X kg-1 X h-1). Picoprazole, a substituted benzimidazole (750 mg/kg), reduced gastric H+ concentration and volume with a rise in K+ concentration [( K+]) to 20–25 meq/l. Insulin alone inhibited acid output to the same extent as Picoprazole but with a marked fall in [K+]. Insulin (0.6 U/kg) given with Picoprazole did not alter inhibition of H+ but prevented the large decrease in gastric juice [K+]. An injection of KCl (1 meq/kg) 1 h after Picoprazole did not alter the effects of the inhibitor. Pepsin secretion after insulin was delayed by Picoprazole, whereas during bethanechol chloride infusion (80 micrograms X kg-1 X h-1) pepsin output was reduced for a shorter period and to a lesser extent than acid. We concluded that insulin affects gastric H+ and K+ secretion by a mechanism not related to H+-K+-ATPase and that Picoprazole affects pepsin secretion probably indirectly via its effect on the parietal cell, where its action is quite consistent with an effect limited to inhibition of the H+-K+-ATPase of the parietal cell.

The Effect of Sub-Threshold Doses of Pentagastrin on the Acid Response to Insulin in Duodenal Ulcer Subjects before and after Truncal Vagotomy

1972 ◽  
Vol 43 (2) ◽  
pp. 201-207 ◽  
Author(s):  
J. B. Elder ◽  
G. Gillespie ◽  
I. E. Gillespie ◽  
G. P. Crean ◽  
A. W. Kay ◽  
...  
Keyword(s):  
Duodenal Ulcer ◽  
Acid Output ◽  
Insulin Response ◽  
Truncal Vagotomy ◽  
Gastric Acid Output ◽  
Cholinergic Stimulation ◽  
Response Curves ◽  
Small Doses ◽  
Before And After ◽  
Threshold Doses

1. On the basis of previously described dose-response curves, small doses of pentagastrin were infused in duodenal ulcer patients before and after vagotomy. No increase or decrease in gastric acid output was noted, confirming that the doses of pentagastrin used were sub-threshold. 2. In twenty-six duodenal ulcer patients the effect of sub-threshold doses of pentagastrin on the insulin response resulted in three distinct patterns. (i) In subjects with clearly functioning vagal pathways, no increase in acid output occurred after insulin when a sub-threshold dose of pentagastrin was added; (ii) patients with equivocal acid responses to insulin alone showed augmentation of acid output when given insulin and a sub-threshold pentagastrin infusion; (iii) patients with no response to insulin after truncal vagotomy showed some increase in acid output to the combined agents, and in two patients, criteria for a clearly positive acid response were satisfied. 3. We conclude from these studies that potentiation exists between insulin-induced cholinergic stimulation and infusion of sub-threshold doses of pentagastrin in man.

Effect of restraint on gastric acidity in the rat

1962 ◽  
Vol 202 (4) ◽  
pp. 812-814 ◽  
Author(s):  
David A. Brodie ◽  
Richard W. Marshall ◽  
Oscar M. Moreno
Keyword(s):  
Gastric Secretion ◽  
Acid Concentration ◽  
Gastric Content ◽  
Free Acid ◽  
Acid Output ◽  
Important Change ◽  
Gastric Fistula ◽  
Total Acid ◽  
Chronic Fistula ◽  
Collection Period

Chronic gastric fistula rats were prepared by implanting stainless steel cannulas in the rumen portion of the stomachs of male Holtzman rats and gastric content was collected in both the unrestrained and restrained state. Gastric secretion in acute pylorus-ligated rats, unrestrained and restrained, was studied at the same time. Volume of gastric content, free and total acidity, and free acid output were significantly lower in the chronic fistula rats as compared to the pylorus-ligated rats in the initial 4-hr collection period. A study of 24-hr gastric content in chronic fistula rats showed that restraint produced a significant decrease in volume, a significant increase in free and total acid concentration, and no change in free acid output, while the restrained pylorus-ligated rats had a significant decrease in volume, no change in free or total acid concentration, and a significant decrease in free acid output as compared with control values. This suggests that an increase in acid concentration is an important change produced in gastric secretion by restraint stress.

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