Gastric Secretion In Dogs Research Articles

Effect of Free Dietary Glutamate on Gastric Secretion in Dogs

The amino acid, L-glutamate, which is abundant in many foodstuffs, is a potent stimulator of gastric vagal afferents. The aim of the study was to evaluate a role of dietary glutamate in neuroendocrine control of gastric secretion of acid, pepsinogen, and fluid. In mongrel dogs with small gastric pouches surgically prepared according to Pavlov (vagally innervated) or Heidenhain (vagally decentralized), secretion in a pouch was induced by infusion into the main stomach of an amino acid-rich diet lacking glutamate (Elental) or the same diet supplemented with monosodium glutamate (MSG). Having no effect alone, MSG (100 mM) potentiated secretion induced by Elental both in Pavlov and Heidenhain models. In the Pavlov pouch, the effect of MSG was markedly reduced after i.v. injection of granisetron, an antagonist of 5-HT(3) receptors. In the Heidenhain model, MSG enhanced the stimulatory effect of pentagastrin (1 microg/kg, s.c.). In conclusion, dietary glutamate at doses not exceeding its common concentrations in foods substantially potentiates gastric phase secretion induced by stimulation of gastric mucosa with an amino acid-rich diet or by administration of pentagastrin. The effect of glutamate is partially mediated via serotonin secretion and stimulation of 5-HT(3) receptors.

Effect of antroneurolysis on gastric secretion in dogs with total gastric fistula.

Abstract The operation of antroneurolysis is performed by circumferential sharp dissection in the submucosal plane of the entire gastric antrum, which severs the vagal nerve-supply to the antral mucosa. It might thus be regarded as a conservative variant of antrectomy, the purpose of which is to diminish gastrin release without disturbing antral peristalsis or the mechanism of the pylorus. Its possible value as an adjunct to highly selective vagotomy in man is evaluated in this study in the dog. The antroneurolysed antrum was left in continuity with the remainder of the stomach whose vagal nerve-supply remained intact. Gastric secretion was collected via a cannula or fistula draining the whole stomach. Outputs of acid and pepsin in response to insulin, pentagastrin, meat extract, and acetylcholine were found to be undiminished after antroneurolysis. It is concluded that antroneurolysis has no place at present in clinical gastric surgery.

Effect of local antihistamines on gastric secretion in dogs.

Effect of local antihistamines on gastric secretion in dogs.

The inhibitory action of a locally applied antihistamine on the antral phase of gastric secretion in dogs.

The inhibitory action of a locally applied antihistamine on the antral phase of gastric secretion in dogs.

Aftect of opioid receptors activation on gastric secretion in dogs

Aftect of opioid receptors activation on gastric secretion in dogs

Aftect of opioid receptors activation on gastric secretion in dogs

Aftect of opioid receptors activation on gastric secretion in dogs

Bile acid inhibits tetragastrin-stimulated gastric secretion after Roux-en-Y biliary diversion in dogs

The present study was carried out to investigate the effect of several bile acids on tetragastrin-stimulated gastric secretion in dogs in which diversion of the biliary system was performed. Cholecystojejunostomy of the Roux-en-Y type was performed, along with the creation of a Heidenhain pouch (HP) and an external duodenal fistula. Gastric juice was collected from the HP and a mixture of bile acids and corn oil was administered through the duodenal fistula. Ursodeoxycholic acid (UDCA) and chenodeoxycholic acid (CDCA) exerted an inhibitory effect on gastric hypersecretion. Conjugated UDCA and several bile acids with different hydroxyl groups were also examined, and these bile acids also showed evidence of an inhibitory effect on the secretion of gastric juice, although there were no significant differences between them. Thus, it appears that all bile acids inhibit tetragastrin-stimulated gastric hypersecretion. This finding suggests that peptic ulcer disease can be prevented by the administration of bile acids to patients who undergo biliary diversion and are at a high risk for this postoperative complication.

Alpha-2 adrenoceptors and gastric secretion in dogs: The role of gastrin

Alpha-2 adrenoceptors and gastric secretion in dogs: The role of gastrin

P-321 - The effect of IGN-2098, a novel H2-blocker, on histamine induced gastric secretion in dogs with Heidenhain pouch

P-321 - The effect of IGN-2098, a novel H2-blocker, on histamine induced gastric secretion in dogs with Heidenhain pouch

Alpha chain unsaturated derivatives of misoprostol

Misoprostol, a 15-deoxy-16-hydroxy-16-methyl analog of PGE 1, is an effective agent for the treatment of peptic ulcer disease. Efforts to impede metabolic degradation of the alpha chain of misoprostol led to the discovery of a second clinical candidate in this series. Enisoprost, a Δ 4Z derivative of misoprostol, is more potent as a gastric antisecretory agent and longer acting than misoprostol. These findings prompted further work to determine the effects that two double bonds in the alpha chain might have on the activity profile of misoprostol. The most promising structure in this series was a 1:1 mixture of 3E, 5z and 3z, 5z dienes which was about three times more potent than misoprostol in inhibiting gastric secretion in dogs, while the separation of the diarrheogenic effect was significantly improved. Chromatographic separation of the mixture was very difficult, but small amounts of each isomer were obtained by HPLC, and preliminary antisecretory studies indicated that most of the activity resided in the 3E, 5Z isomer. A stereospecific synthesis of the 3E, 5z isomer was carried out to provide sufficient quantities for complete pharmacological assessment. The 3E, 5z diene was about three times more potent than misoprostol in inhibiting gastric acid secretion in dogs and also in producing diarrhea in rats.

Mechanisms of gastric secretion in dogs induced by infusion of histamine, carbachol, and pentagastrin

Mechanisms of gastric secretion in dogs induced by infusion of histamine, carbachol, and pentagastrin

The Effect of Chemical Sympathectomy on Insulin-Stimulated Gastric Secretion in Dogs

Administration of 6 hydroxydopamine (6 OHDA) causes selective acute degeneration of the adrenergic nerve terminals, that is a reversible chemical sympathectomy. The effect of this drug was studied on the insulin stimulated gastric secretion. Insulin stimulated (0.15-0.4 IU/kg) gastric acid and pepsin output and serum gastrin was measured before and after 6 OHDA treatment (40 mg/kg) in gastric fistula dogs. Chemical sympathectomy resulted in a highly significant increase in acid and pepsin secretion. However, the hypoglycemic gastrin release was unaltered except the peak response, which showed a significant reduction. These data confirm earlier observations, that the sympathetic innervation of the stomach has an inhibitory effect on gastric secretion in the dog. Furthermore it seems that the adrenergic fibres in the vagus nerve might have some moduling effect on the insulin induced gastrin release.

Role of antral mucosa in intestinal phase of gastric secretion in dogs.

This study was performed to investigate the mechanisms and significance of the intestinal phase of gastric secretion. With infusion of 10% liver extract into the duodenum of dogs, serum gastrin levels of the right gastroepiploic vein increased significantly (p less than 0.01). With infusion of the pH 7.0 liver extract, acid and pepsin outputs in non- antrectomized dogs increased significantly (p less than 0.01), as did serum gastrin levels (p less than 0.01). Post-infusion acid output in these dogs was 48 +/- 16% of tetragastrin-stimulated output. With the same infusion, antrectomized dogs showed no significant increase of acid and pepsin outputs and serum gastrin levels. Acid output and serum gastrin levels in non- antrectomized dogs that were infused with pH 2.0 liver extract did not increase significantly. The values of almost all serum amino acids in both types of dogs increased slightly, but insignificantly, with pH 7.0 liver extract. We obtained the following conclusions. The intestinal phase of gastric secretion operates by the mediation of the antral mucosa, from which gastrin is released. Although this phase has some effect, the acid-secretory ability of this phase is masked by inhibitory systems under certain physical conditions.

Effect of pancreatic juice on basal pancreatic and gastric secretion in dogs.

1. The effect of duodenal infusion of pancreatic juice on basal pancreatic and gastric secretion was studied in five conscious dogs provided with pancreatic fistulae, gastric fistulae and Heidenhain fundic pouches. 2. Pancreatic juice and trypsin stimulated a pancreatic secretion rich in protein. 3. Autodigested juice without proteolytic activities also stimulated the secretion. Boiling the juice or addition of trypsin inhibitor to the juice diminished the augmented secretion. 4. It seems, therefore, that trypsin is necessary even in proteolytically inactive autodigested juice for pancreatic stimulation. 5. In dogs, unlike rats and pigs, basal pancreatic secretion is not under negative feed-back control by duodenal tryptic activity. 6. Basal gastric secretion was not significantly changed by duodenal infusion of pancreatic juice.

Effect of 3-isobutyl-1-methylxanthine on histamine-stimulated gastric secretion in dogs.

The effect of IMX on histamine-stimulated gastric secretion has been studied in dogs equipped with gastric cannulas. After determining the histamine dose response, IMX, histamine, and IMX plus histamine were given by a constant intravenous infusion for 3 h, and acid was collected at 15-min intervals. In a separate series of experiments a single dose of 100 mg of db-cAMP was given 1 h after initiation of infusion of IMX, histamine, and histamine plus IMX. Results show that IMX, a potent inhibitor of phosphodiesterase, is a weak stimulant of acid secretion, and augments histamine-stimulated secretion. However, during stimulated acid secretion, there were no significant changes in tissue cAMP levels, Administration of exogenous dib-cAMP did not produce any significant changes in acid secretion in dogs, but did contribute to elevated cAMP levels.

The effect of propranolol on insulin-stimulated gastric secretion in dogs.

The effect of beta-adrenergic blockade on the insulin hypoglycemia-induced gastric secretion was studied. Insulin-stimulated (0.15 IU/kg) gastric acid and pepsin output and serum gastrin were measured before and after beta-adrenergic blockade with propranolol (20 microgram/kg/min intravenous infusion) in gastric fistula and Heidenhain pouch dogs. Insulin injection caused acid and pepsin secretion from the gastric fistula, and both acid and pepsin secretion was significantly increased during beta-adrenergic blockade. Significant gastrin release was observed after insulin stimulation. However, the insulin-induced gastrin release was unaltered by intravenous infusion of propranolol. The Heidenhain pouch did not show any secretion in these experiments. It is concluded that beta-adrenergic blockade augments the hypoglycemia-induced gastric secretion in dogs. Furthermore, it seems that this effect is not dependent on vagally released gastrin.

Inhibitory action of methionine-enkephalin and morphine on pentagastrin-stimulated gastric secretion in dogs

Inhibitory action of methionine-enkephalin and morphine on pentagastrin-stimulated gastric secretion in dogs

A study of gastric secretion in dogs using pilocarpine.

1 Pilocarpine (40 microgram/min i.v.) stimulated acid and pepsin secretion from Heidenhain pouches but did not stimulate secretion from the innervated stomach. 2 Pilocarpine significantly increased acid secretion from the innervated main stomach after the vagal nerves were bilaterally blocked with lidocaine. 3 The effect of pilocarpine on secretion from the Heidenhain puch was depressed by ganglionic blockade (hexamethonium), by dopamine and by isoprenaline. 4 The stimulatory action of histamine on gastric secretion from either pouch or gastric fistulae was uninfluenced by dopamine. 5 The action of pilocarpine was augmented by the muscarinic ganglionic stimulant AHR 602. Considering this effect, as well as the secretory depression of isoprenaline, pilocarpine resembles pentagastrin rather than methacholine in its action.

Inhibitory effect of leu-enkephalin on gastric secretion in dogs

Association potentialities of acrocentric chromosomes were evaluated from the frequencies of associations consisting of two homologues. The evidence obtained enabled one to calculate the frequencies of associations consisting of two nonhomologous and mixed acrocentric chromosomes. Such frequencies turned out to occur 4-fold less than empiric frequencies of the respective associations. This is possible with 2-fold increase in the association potentialities of each acrocentric chromosome entering the association of two nonhomologous and mixed chromosomes. A correlation performed according to Pirson's criterion revealed a good agreement of empiric and theoretic frequencies calculated with due regard 2-fold magnification of the association potentialities. This finding does not reject a hypothesis of 2-fold magnification of the association potentialities in acrocentric chromosomes entering the association consisting of 2 non-homologous and mixed chromosomes.

Non-gastrin, intestinal-phase secretion. Experimental confirmation in the dog.

Four mongrel dogs were prepared with a Heidenhain pouch, a gastric fistula, and a 90-cm-long Thiry-Vella loop. After recovery, dose-response curves were obtained with different doses of pentagastrin, and the maximal acid output was determined. The jejunal loop was perfused for 3 h with either 5% liver extract or with 0.15 M NaCl at a rate of 114 ml/h. To verify that the stomach could release gastrin and that the assay could detect that change, antral perfusion with liver extract was performed. Serum gastrin levels and acid output were measured every 30 min. Perfusion of the jejunal loop with liver extract resulted in a significant increase in acid output from the Heidenhain pouch and the gastric fistula, whereas perfusion with saline solution failed to show any changes. The magnitude of acid response from the Heidenhain pouch and gastric fistula was 11% and 18%, respectively, as compared with maximal pentagastrin stimulation. The serum gastrin levels remained unchanged during both liver extract and saline perfusion of the jejunal loop, in contrast to the marked increase in serum gastrin level after antral perfusion. The results confirm the existence of the intestinal phase of gastric acid stimulation in dogs as an entity and show that the magnitude of this phase is significantly lower than has been suggested by results of earlier studies. Furthermore, the results suggest that the intestinal phase of gastric secretion in dogs is most probably elicited through a humoral agent other than gastrin.