Inhibition of cephalic and antral phases of gastric secretion by antral chalone

1962 ◽  
Vol 202 (4) ◽  
pp. 716-720 ◽  
Author(s):  
James C. Thompson ◽  
Harvey J. Lerner ◽  
Jorge A. Tramontana
Keyword(s):  
Hydrochloric Acid ◽  
Gastric Secretion ◽  
Portal Vein ◽  
Acid Secretion ◽  
Acid Output ◽  
Insulin Hypoglycemia ◽  
Heidenhain Pouch ◽  
Pavlov Pouch

The effect of antral acidification on the antral and cephalic phases of gastric secretion has been studied. Cross-transfusions were carried out between pairs of dogs in which blood from the portal vein of one dog was administered to another dog with a denervated fundic pouch. Transfusion of blood collected during acidification of the antrum resulted in a diminution of Heidenhain pouch acid secretion in response to food and to topical acetylcholine of 64% and 83%, respectively. The effect of antral acidification on gastric secretion stimulated by insulin hypoglycemia was studied in dogs prepared with Pavlov and isolated antral pouches (innervated and denervated). Irrigation of the antral pouch with .1 n hydrochloric acid resulted in a 92% decrease in Pavlov pouch acid output.

Effects of bombesin on food intake and gastric acid secretion in cats

1989 ◽  
Vol 256 (1) ◽  
pp. R181-R186
Author(s):  
A. Bado ◽  
M. J. Lewin ◽  
M. Dubrasquet
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Gastric Secretion ◽  
Acid Secretion ◽  
Gastric Fistula ◽  
Single Class ◽  
Heidenhain Pouch ◽  
Daily Food Intake ◽  
Feeding Experiments ◽  
Daily Food

The brain and gut peptide bombesin has been reported both to stimulate gastric secretion and to induce satiety. To understand how the peripheral administration of bombesin affects food intake and whether gastric mechanisms are involved, a comparative study of the doses of bombesin active on gastric secretion, gastric emptying, and food intake was undertaken in cats provided with a gastric fistula and a denervated Heidenhain pouch. The smallest dose of intravenous bombesin that stimulated significantly basal acid secretion (20 pmol.kg-1.h-1) by the gastric fistula also enhanced meal-stimulated acid secretion by the Heidenhain pouch (+138%, P less than 0.01), delayed gastric emptying of a liquid protein meal (-30%, P less than 0.01), and suppressed food intake when the test meal was allowed to reach the stomach (-15%, P less than 0.01). Conversely, in sham-feeding experiments, the same dose of bombesin increased food intake (+35%, P less than 0.01). In full-day experiments conducted in nonfasted cats, bombesin decreased both the food intake in the 4-h period after the infusion and the daily food intake, whereas octapeptide cholecystokinin induced a transient satiety but did not decrease daily food intake. These results indicate that in cats the interaction of bombesin with "pregastric" mechanisms is not sufficient to induce satiety and that a relation could exist between the effects of bombesin on gastric secretion, emptying, and food intake. A single class of receptors might be involved in these peripheral effects of bombesin.

Response of chronic denervated gastric pouches of rats to food and histamine

1962 ◽  
Vol 203 (4) ◽  
pp. 641-643 ◽  
Author(s):  
R. S. Alphin ◽  
T. M. Lin
Keyword(s):  
Hydrochloric Acid ◽  
Gastric Secretion ◽  
Acid Secretion ◽  
Dose Range ◽  
Gastric Pouch ◽  
Free Base ◽  
Conscious Rat ◽  
Volume Output ◽  
Dose Levels

The volume output and hydrochloric acid secretion from the denervated gastric pouch of the rat in response to food and histamine were studied. Food was given at three dose levels—1.25, 2.5, and 5.0 g—and histamine (as free base) was given subcutaneously at dose levels of 0.34, 0.7, 1.4, and 2.8 mg/kg. The results show that the chronic denervated gastric pouch of the rat responds in a graded manner to both food and histamine in a certain dose range. Although rats are not as sensitive to histamine as humans and dogs, the chronic gastric pouch of the conscious rat is far more sensitive to histamine than the stomach of the pyloric-ligated or anesthetized rat. The feasibility of using this preparation for testing the effect of agents inhibiting food- or histamine-stimulated gastric secretion is discussed.

Secretin effect on gastrin, gastric secretion in dogs with chronic antral stimulation

1975 ◽  
Vol 228 (6) ◽  
pp. 1775-1781 ◽  
Author(s):  
S Nasca ◽  
M Mignon ◽  
L Gramatica ◽  
J-P Accary ◽  
S Bonfils
Keyword(s):  
Gastric Secretion ◽  
Acid Output ◽  
Physiological Activity ◽  
Fold Increase ◽  
Acid Inhibition ◽  
Plasma Gastrin ◽  
Heidenhain Pouch ◽  
Fasting Plasma

Antrocolic transposition in four dogs with Heidenhain pouch and gastrojejunostomyresulted in a marked increase in fasting plasma gastrin concentration and sustained highacid secretion, closely related to gastrin levels. A marked production of pepsin output could not be correlated with plasma gastrin. Reduction in plasma gastrin concentration was more than twofold less pronounced than the reduction in acid output for 1 and 2 U/kg-h, while the 0.5 U/kg-h no effect was noted. For both acid output and gastrin concentrations, close correlations were noted between presecretion level and remaining level upon secretin infusion. Despite the reduction in the secretory volume of the pouch, 0.5 and 1 U/kg-h of secretin induced a 1.5- and 2-fold increase in pepsin output, respectively. Two untis per kilagram-hour decreased the secretory volume as well as the pepsin output. If the physiological release of secretin in dogs does not exceed the equivalent of the lowest dose studied, our results would indicate that acid inhibition is a physiological activity of secretin, while the effect on circulating gastrin concentration seems to be phamacological.

Inhibitory Effect of Pancreatic Secretin on Gastric Secretion

1957 ◽  
Vol 190 (3) ◽  
pp. 396-402 ◽  
Author(s):  
Herbert B. Greenlee ◽  
Enrique H. Longhi ◽  
Jose Delgadillo Guerrero ◽  
Thomas S. Nelsen ◽  
Abdul Latif El-Bedri ◽  
...  
Keyword(s):  
Gastric Secretion ◽  
Intravenous Injection ◽  
Inhibitory Effect ◽  
The Other ◽  
Gastrin Release ◽  
Depressant Effect ◽  
Insulin Hypoglycemia ◽  
Heidenhain Pouch ◽  
Marked Inhibition ◽  
Inhibition Of Gastric Secretion

In dogs prepared with both a vagus denervated Heidenhain pouch and a total pancreatic fistula, the intravenous injection of pancreatic secretin (Lilly) produced a profuse secretion of pancreatic juice and a simultaneous marked inhibition of gastric secretion. In dogs prepared with an isolated antrum pouch and a Heidenhain pouch the gastric secretion induced by the instillation of food in the antrum pouch was completely inhibited by the intravenous injection of pancreatic secretin. On the other hand, the intravenous injection of pancreatic secretin had little or no effect on the secretion of gastric juice produced by insulin hypoglycemia or by the injection of histamine. It is suggested that pancreatic secretin may represent the mechanism by means of which acid food in the duodenum inhibits gastric secretion. It is probable that this inhibition is caused by prevention of gastrin release from the antrum rather than to a depressant effect on the parietal cells.

Effect of thiamine deficiency on canine gastric secretion of acid

1959 ◽  
Vol 197 (2) ◽  
pp. 253-256 ◽  
Author(s):  
Marjorie K. Lavers ◽  
Patricia A. Stefanik ◽  
Charles F. Code
Keyword(s):  
Body Weight ◽  
Hydrochloric Acid ◽  
Gastric Mucosa ◽  
Gastric Secretion ◽  
Thiamine Deficiency ◽  
Acid Output ◽  
Nervous Stimulation ◽  
Deficiency State ◽  
Bethanechol Chloride ◽  
Secretory Capacity

A study was undertaken to determine the effect of thiamine deficiency on the hydrochloric acid output of vagally denervated gastric pouches (Heidenhain-type) and vagally innervated gastric pouches (Pavlov-type) in dogs. Responses of both types of pouches to injection of 0.05 mg of histamine/kg of body weight and the maximal secretory capacity of both types after histamine were unaltered during the deficiency state. A degree of thiamine deficiency sufficient to produce anorexia and neuritis was without effect on the secretory response of canine gastric mucosa to histamine. The hydrochloric acid output of vagally innervated pouches during nervous stimulation caused by insulin-induced hypoglycemia was drastically reduced as soon as thiamine deficiency developed, while the response to bethanechol chloride was little, if at all, affected. It is concluded that the vagal secretory mechanism participates in the general neural failure of thiamine deficiency and that this failure most likely is in the neurons of the vagal nuclei.

Effect of GABA on basal and vagally mediated gastric acid secretion and hormone release in dogs

1988 ◽  
Vol 254 (5) ◽  
pp. G723-G731
Author(s):  
R. C. Thirlby ◽  
M. H. Stevens ◽  
A. J. Blair ◽  
F. Petty ◽  
I. L. Crawford ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Blood Brain Barrier ◽  
Gaba Receptors ◽  
Gaba Receptor ◽  
Receptor Agonist ◽  
Acid Output ◽  
Gastric Fistula ◽  
Heidenhain Pouch

To stimulate peripheral gamma-aminobutyric acid (GABA) receptors, GABA, which does not cross the blood-brain barrier, was administered to dogs with vagally innervated gastric fistulas at intravenous doses of 0, 0.66, 2, 6, 18, and 54 micrograms.kg-1.min-1. Mean gastric acid output increased from zero basally to 3.0 +/- 1.4 mmol/h during infusion of 54 micrograms.kg-1.min-1 GABA. Plasma somatostatin-like immunoreactivity decreased significantly below basal levels during infusion of 54 micrograms.kg-1.min-1 GABA (P less than 0.05). To stimulate central nervous system GABA receptors as well as peripheral GABA receptors, progabide, a GABA-receptor agonist, which readily crosses the blood-brain barrier, was injected intravenously. Mean acid output was 3.5 +/- 1.3 mmol/h after 20 mg/kg progabide and 0.6 +/- 0.5 mmol/h after its vehicle (P less than 0.05). Basal serum gastrin concentration increased significantly after progabide injection. Acid output during insulin-induced hypoglycemia was inhibited 59% by 30 mg/kg intravenous progabide. Progabide infusion also diminished or abolished circulating gastrin, somatostatin, and pancreatic polypeptide responses during insulin-induced hypoglycemia (P less than 0.05). Further studies were performed in dogs with a gastric fistula and a vagally denervated Heidenhain pouch to confirm that GABA-receptor stimulation affects acid secretion via peripheral pathways. Intravenous injection of baclofen (0.5 mg/kg), a GABAB-receptor agonist, increased acid secretion significantly from the gastric fistula and the Heidenhain pouch. These studies suggest that GABA may play a role in regulating gastric acid secretion and gastrointestinal and pancreatic endocrine function by both central and peripheral mechanisms.

Serotonin release by hydrochloric acid: possibility of a feed-back mechanism

1961 ◽  
Vol 201 (6) ◽  
pp. 1017-1019 ◽  
Author(s):  
Robert H. Resnick ◽  
Seymour J. Gray
Keyword(s):  
Hydrochloric Acid ◽  
Gastric Secretion ◽  
Portal Vein ◽  
Serotonin Release ◽  
Secretory Function ◽  
Drug Induced ◽  
Rat Portal Vein ◽  
Inhibition Of Gastric Secretion ◽  
Intestinal Serotonin ◽  
Partial Depletion

This investigation was carried out to determine whether the release of upper intestinal serotonin produced by hydrochloric acid perfusion was responsible for a subsequent inhibition of gastric secretion. To explore this possibility, gastric secretion in the pyloric-ligated rat was studied after the administration of varying quantities of serotonin through the rat portal vein. In another series of tests, the capacity of intestinally perfused hydrochloric acid to inhibit gastric secretion was studied in animals partially depleted of serotonin by reserpine or subjected to drug-induced chemical blockade of serotonin effect. Results indicate that serotonin infused through the portal vein does not alter gastric pH or secretory volume and that partial depletion of tissue serotonin or the use of serotonin antagonists does not prevent the intestinal suppression of gastric secretory function. It is therefore concluded that the intestinal release of serotonin is not a factor in the reduction of gastric acidity after HCl perfusion of the small intestine.

scholarly journals Role of Na-K-2Cl cotransporter-1 in gastric secretion of nonacidic fluid and pepsinogen

2005 ◽  
Vol 289 (3) ◽  
pp. G550-G560 ◽  
Author(s):  
Nichole McDaniel ◽  
Amy J. Pace ◽  
Stefanie Spiegel ◽  
Regina Engelhardt ◽  
Beverly H. Koller ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Gastric Secretion ◽  
Acid Secretion ◽  
Acid Output ◽  
Gastric Gland ◽  
Electrical Current ◽  
Fluid Secretion ◽  
Parietal Cells ◽  
Pepsinogen Secretion ◽  
Deficient Mice

Na-K-2Cl cotransporter-1 (NKCC) has been detected at exceptionally high levels in the gastric mucosa of several species, prompting speculation that it plays important roles in gastric secretion. To investigate this possibility, we 1) immunolocalized NKCC protein in the mouse gastric mucosa, 2) compared the volume and composition of gastric fluid from NKCC-deficient mice and their normal littermates, and 3) measured acid secretion and electrogenic ion transport by chambered mouse gastric mucosa. NKCC was localized to the basolateral margin of parietal cells, mucous neck cells, and antral base cells. In NKCC-deficient mice, gastric secretions of Na+, K+, Cl−, fluid, and pepsinogen were markedly impaired, whereas secretion of acid was normal. After stimulation with forskolin or 8-bromo-cAMP, chambered corpus mucosa vigorously secreted acid, and this was accompanied by an increase in transmucosal electrical current. Inhibition of NKCC with bumetanide reduced current to resting levels but had no effect on acid output. Although prominent pathways for basolateral Cl− uptake (NKCC) and apical Cl− exit [cystic fibrosis transmembrane conductance regulator (CFTR)] were found in antral base cells, no impairment in gastric secretion was detected in CFTR-deficient mice. Our results establish that NKCC contributes importantly to secretions of Na+, K+, Cl−, fluid, and pepsinogen by the gastric mucosa through a process that is electrogenic in character and independent of acid secretion. The probable source of the NKCC-dependent nonacidic electrogenic fluid secretion is the parietal cell. The observed dependence of pepsinogen secretion on NKCC supports the concept that a nonacidic secretory stream elaborated from parietal cells facilitates flushing of the proenzyme from the gastric gland lumen.

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