Gastric effects of TRH analogue and bicuculline injected into dorsal motor vagal nucleus in cats

1990 ◽  
Vol 259 (2) ◽  
pp. G321-G326 ◽  
Author(s):  
H. S. Feng ◽  
R. B. Lynn ◽  
J. Han ◽  
F. P. Brooks
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Motor Nucleus ◽  
Inhibitory Influence ◽  
Gastric Acid Output ◽  
Minimal Effective Dose ◽  
Gabaa Receptor Antagonist ◽  
Dose Dependent

We investigated the gastric acid secretory and motility responses to microinjection into the dorsal motor nucleus of the vagus (DMV) of RX 77368, a stable thyrotropin-releasing hormone (TRH) analogue, and bicuculline, a gamma-aminobutyric acid (GABAA) receptor antagonist in ketamine-chloralose-anesthetized cats. Gastric acid output was collected every 15 min through a gastric cannula after saline flush and titrated to pH 7.0. Antral contractions were continuously recorded by an extraluminal strain gauge force transducer. The chemicals were dissolved in saline and unilaterally microinjected in volumes of 200 nl. RX 77368 or bicuculline microinjected into the DMV induced significant dose-dependent (50-500 ng) increases in gastric acid secretion and significant dose-dependent (50-200 ng) increases in the force of antral contractions. In response to both chemicals the gastric acid output increased in the first 15 min and peaked in the second and third collections. RX 77368 (500 ng) had a second greater peak 90 min after microinjection. The motility responses were rapid in onset and lasted 60 min for RX 77368 and 30 min for bicuculline. The minimal effective dose for eliciting increased motility was consistently lower than inducing acid secretion. Electrical stimulation of the DMV with 100 microA, 50-Hz, and 0.2-ms pulse duration increased the force of antral contractions but had no effect on gastric acid secretion. Our results demonstrate that the DMV exerts important control over both gastric acid secretion and motility in cats. TRH exerts a stimulatory influence, while GABAA receptors mediate an inhibitory influence on this vagal control.

Ventromedial hypothalamic lesions elevate basal and cephalic phase gastric acid output

1980 ◽  
Vol 239 (3) ◽  
pp. G221-G229 ◽  
Author(s):  
H. P. Weingarten ◽  
T. L. Powley
Keyword(s):  
Weight Gain ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Gastric Acid Output ◽  
Full Development ◽  
Cephalic Phase ◽  
A New Technique ◽  
Induced Changes

With the use of a new technique for the measurement of gastric acid output in the rat, this study identifies ventromedial hypothalamic (VMH) lesion-induced changes in gastric acid secretion. Basal and cephalic phase gastric acid secretion were monitored in VMH- and sham-lesioned control rats on days 1, 5, 9, 13, and 17 postlesion as well as after the full development of obesity. VMH lesions resulted in increases of both phases of secretion. The magnitude of hypersecretion in lesioned rats developed with time and was fully developed by day 9 postlesion. The hypersecretion did not require a hyperphagia or weight gain, but its degree correlated with subsequent weight gain. These data, in conjunction with a review of VMH lesion effects on insulin secretion, suggest a widespread effect of VMH lesions on visceral secretory responses. The relevance of these data to the etiology of the VMH syndrome is discussed.

scholarly journals Acute Effect of Gamma Irradiation on Gastric Acid Secretion and Gastric Mucosal Integrity in the Rat

2005 ◽  
Vol 5 ◽  
pp. 195-204
Author(s):  
Omar M. E. Abdel Salam ◽  
Ihsan Hadajat ◽  
Ayman Ragab Bayomy ◽  
Siham El-Shinawy ◽  
Mahmoud S. Arbid
Keyword(s):  
Acid Secretion ◽  
Gamma Irradiation ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Whole Body ◽  
Mucosal Barrier ◽  
Dependent Manner ◽  
Gastric Acid Output ◽  
Direct Stimulation

The effect of 3- or 6-Gray (Gy) whole-body gamma irradiation on basal and stimulated gastric acid secretion was studied in pylorus-ligated rats. Different groups of rats were irradiated with a single 3- or 6-Gy fraction and examined 7 days after irradiation. Exposure to 3-Gy fraction led to marked increase in basal (nonstimulated) gastric acid output in the 4-h pylorus-ligated rat (47.5% compared with unirradiated controls). After exposure to 6 Gy, only 18.2% increase in gastric acid output was noted compared with unirradiated controls. Under pentagastrin or histamine stimulation, gastric acid secretion in those irradiated with 3- or 6-Gy fraction was markedly reduced compared to that of unirradiated controls. Exposure to 3- or 6-Gy gamma irradiation intensified the degree of gastric mucosal injury evoked by indomethacin or 50% ethanol in a dose-dependent manner. It is concluded that in the pylorus-ligated rat model, lower doses of gamma irradiation increase basal gastric acid secretion and impair the gastric mucosal barrier with marked increase in its permeability to H+following stimulation of acid secretion or exposure to barrier breakers. Exposure to irradiation is likely to result in failure of the parietal cell to respond to direct stimulation with histamine or pentagastrin.

Dissociated effects of somatostatin on gastric acid secretion and mucosal blood flow

1985 ◽  
Vol 248 (3) ◽  
pp. G337-G341
Author(s):  
F. W. Leung ◽  
P. H. Guth
Keyword(s):  
Blood Flow ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Mucosal Blood Flow ◽  
Hydrogen Gas ◽  
Gastric Acid Output ◽  
Hydrogen Gas Clearance ◽  
Blood Flows

Somatostatin has been reported to control upper gastrointestinal hemorrhage, prevent restraint stress-induced gastric ulcerations, and inhibit gastric acid secretion. In this study we examined the effect of somatostatin on basal and pentagastrin-stimulated gastric acid output and mucosal blood flow. Antral and corpus mucosal blood flows were measured by hydrogen gas clearance in fasted, anesthetized rats. Acid output was determined by a continuous gastric perfusion technique. In the basal study somatostatin in doses of 8, 16, and 32 micrograms . kg-1 . h-1 was infused intravenously in separate groups of animals. In the pentagastrin stimulation study somatostatin (16 micrograms . kg-1 . h-1) was infused after gastric acid output was stimulated to plateau by intravenous pentagastrin (19.8 micrograms . kg-1 . h-1). The results showed that somatostatin had no effect on basal corpus or antral mucosal blood flow. During pentagastrin stimulation somatostatin decreased acid secretion but increased corpus mucosal blood flow. We speculate that this increase in blood flow may not be a direct effect as basal corpus or antral mucosal blood flow was unaffected by somatostatin.

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.

5-CT or DOI augments TRH analog-induced gastric acid secretion at the dorsal vagal complex

1997 ◽  
Vol 273 (5) ◽  
pp. R1607-R1611 ◽  
Author(s):  
Sridhar Varanasi ◽  
Jinhan Chi ◽  
Robert L. Stephens
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Serotonin Receptor ◽  
Acid Output ◽  
Receptor Subtypes ◽  
Dorsal Vagal Complex ◽  
Gastric Acid Output ◽  
Integrated Response ◽  
Sc 53116

Serotonin (5-HT) interacts with thyrotropin-releasing hormone (TRH) at the dorsal vagal complex (DVC) to augment TRH-induced stimulation of gastric acid secretion. To investigate the 5-HT receptor family involved in the augmentation response, prototypical 5-HT receptor-selective agonists (146 pmol) were coinjected with the TRH analog RX-77368 (RX; 12 pmol) into the rat DVC in a 30-nl volume. The DVC coordinates were 0.2 mm anterior, 0.2 mm right, 0.6 mm ventral with respect to the calamus scriptorius. Coinjection of RX with the 5-HT agonists 5-carboxyamidotryptamine (5-CT) or (±)-1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride (DOI; 5-HT2 agonist) produced a 183 or 103% increase in gastric acid output compared with the RX injection alone. In contrast, coinjection of 2- methyl-5-HT (5-HT3 agonist) with RX produced no effect on RX-induced increase in gastric acid secretion. Moreover, coinjection of SC-53116 (5-HT4agonist) decreased the gastric acid output by 45% compared with the RX response itself. Examination of the RX/5-HT agonist coinjection response in more rostral regions of the DVC using the same doses (5-CT/RX or DOI/RX) revealed that only 5-CT was effective in producing the augmented response to TRH analog. The results suggest that activation of 5-CT- or DOI-sensitive receptors augments, and of 5-HT4 receptors inhibits, the gastric acid response to TRH analog injected into the DVC. Thus the integrated response to several serotonin receptor subtypes may mediate changes to the TRH response induced by 5-HT at the DVC.

5-HT in DVC: disparate effects on TRH analogue-stimulated gastric acid secretion, motility, and cytoprotection

1996 ◽  
Vol 271 (2) ◽  
pp. R368-R372 ◽  
Author(s):  
J. Chi ◽  
J. Kemerer ◽  
R. L. Stephens
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Gastric Acid Output ◽  
Cytoprotective Effect ◽  
Gastric Mucosal Lesions ◽  
Antral Motility ◽  
Mucosal Lesions ◽  
Stimulation Of

Convergent evidence suggests that thyrotropin-releasing hormone (TRH) is a principal regulator of several vagally mediated gastric responses. Serotonin (5-HT) interacts with TRH in the dorsal vagal complex (DVC) to augment gastric acid secretory responses. This study investigated the ability of 5-HT to alter other gastric responses mediated by TRH administration into the DVC. Co-injection of 5-HT (7.9 pmol) and the TRH analogue RX-77368 (0.66 pmol) produced a 117% enhancement in 1-h gastric acid output compared with rats treated with RX-77368 (0.66 pmol) alone into the DVC. In contrast, coadministration of RX-77368 (4 pmol) with various doses of 5-HT (0.0048-480 pmol) was ineffective in significantly altering stimulation of gastric antral motility produced by RX-77368 (4 pmol) alone. The effect of a lower dose of DVC RX-77368 (0.66 pmol) on gastric motility was also not changed by 5-HT coadministration. Moreover, the cytoprotective effect of DVC RX-77368 (1.5 pmol) on oral ethanol-induced gastric mucosal lesions was reversed by 5-HT coadministration (54 or 18 pmol). The results suggest that activation of 5-HT receptors in the DVC can augment, not affect, and attenuate DVC TRH analogue-stimulated gastric acid secretion, antral motility, and cytoprotection, respectively.

scholarly journals Dihydroquercetin (taxifolin) attenuates dexamethasone activity on prostaglandin E-2 but potentiates thromboxane-A2 action in gastric acid secretion in wistar rats

2020 ◽  
Vol 13 (3) ◽  
pp. 181-188
Author(s):  
Etah Etah Nkanu
Keyword(s):  
Body Weight ◽  
Prostaglandin E2 ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Wistar Rats ◽  
Acid Output ◽  
Thromboxane A2 ◽  
Mucus Secretion ◽  
Gastric Acid Output

The activity of dexamethasone and taxifolin {(2R, 3R)-2-(3, 4-Dihydroxyphenyl)-3,5,7-trihydroxy-2,3-dihydrochromen-4-one}supplementation on prostaglandin E2 and thromboxane A2 in gastric acid secretion and anti-ulcer was studied. Twenty male Wistar rats (180g-200g body weight) were used. The rats were randomly selected into four groups containing 5 rats each. Group 1 was the control group fed on normal rat feed. Group 2 received 3mg/kg of Dexamethasone (intraperitoneally) at one day interval. Group 3 received 3mg/kg of Dex. intraperitoneally and 1mg/kg body weight of taxifolin orally while group 4 received 1mg/kg body weight of taxifolin. At the end of 6 weeks, basal and peak gastric acid output was measured by continuous perfusion of rats stomach under anaesthesia with normal saline at the rate of 1ml/min. Gastric acid, mucus secretion, ulcer index, PGE-2 and thromboxane A2 activity were determined according to standard procedures. Results showed a significantly (p<.05) decreased prostaglandin and mucus secretion level and a raised thromboxane concentrations and gastric acid output in dexamethasone administration. Taxifolin significantly (p<.05) lowered thromboxane A2 concentration in Dex treatment while increasing the prostaglandin E2 level. We conclude that Taxifolin decreases dexamethasone- induced gastric acid secretion, increases prostaglandin activity but reduces thromboxane concentration.

Effect of hyperglycemia on gastric acid secretion during the gastric phase of digestion

1997 ◽  
Vol 272 (5) ◽  
pp. G1116-G1121 ◽  
Author(s):  
W. F. Lam ◽  
A. A. Masclee ◽  
E. S. Muller ◽  
C. B. Lamers
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Pancreatic Polypeptide ◽  
Acid Output ◽  
Serum Glucose ◽  
Phenol Red ◽  
Gastrin Release ◽  
Gastric Acid Output ◽  
Liquid Meal

We have examined the effect of an acute stable hyperglycemia on gastric acid secretion during the gastric phase of digestion. Gastric acid output was measured with a recovery marker (phenol red) under basal conditions and after repeated intragastric instillation of a liquid meal in seven healthy subjects on two separate occasions: during normoglycemia (serum glucose, 15 mM). Premeal gastric acid output was significantly (P < 0.05) reduced during hyperglycemia compared with during normoglycemia (2.6 +/- 1.0 vs. 5.8 +/- 1.8 mmol/h). Intragastric meal-stimulated incremental acid output during hyperglycemia was significantly (P < 0.05) reduced compared with during normoglycemia (19 +/- 4 vs. 38 +/- 9 mmol/120 min). Meal-stimulated gastrin release during hyperglycemia was significantly (P < 0.05) reduced compared with that during normoglycemia (4.9 +/- 1.3 vs. 6.6 +/- 1.6 micrograms.1(-1).120 min-1). The intragastric meal induced significant (P < 0.05) increases in pancreatic polypeptide concentrations only during normoglycemia. During hyperglycemia, recovery rates of gastric contents were significantly (P < 0.05) increased compared with during normoglycemia, both before (81 +/- 4 vs. 71 +/- 6%) and after (72 +/- 4 vs. 57 +/- 4%) meal ingestion, pointing to delayed gastric emptying of liquids during hyperglycemia. In conclusion, 1) gastric acid secretion under unstimulated conditions and during the gastric phase of digestion is reduced during hyperglycemia; 2) meal-stimulated gastrin release is significantly reduced during hyperglycemia; 3) the reduction in meal-stimulated acid output is correlated with the reduction in gastrin releases; and 4) pancreatic polypeptide secretion is significantly reduced during hyperglycemia, pointing to impaired vagal cholinergic tone.

Modulation of gastric acid secretion by adenosine in conscious rats

1987 ◽  
Vol 65 (6) ◽  
pp. 1182-1185 ◽  
Author(s):  
G. B. Glavin ◽  
V. S. Westerberg ◽  
J. D. Geiger
Keyword(s):  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Adenosine Receptor ◽  
Acid Output ◽  
Gastric Acid Output ◽  
Gastric Function ◽  
Conscious Rats ◽  
Adenosine Receptor Antagonist

Basal (nonstimulated) gastric acid output was determined in conscious rats fitted with indwelling gastric cannulae. The adenosine deaminase resistant analog of adenosine, R-phenylisopropyladenosine, elevated intraluminal pH beyond 7.0 and decreased gastric acid secretion when given at doses of 0.10 or 1.0 mg/kg, while S-phenylisopropyladenosine at similar doses did not affect either gastric acid output or pH. The potent adenosine receptor antagonist, 8-phenyltheophylline, given at doses of 0.1, 1.0, and 2.5 mg/kg augmented gastric acid output and, at doses of 0.01, 0.1,1.0, and 2.5 mg/kg, blocked the acid-reducing effect of R-phenylisopropyladenosine (0.1 mg/kg). These data suggest that adenosine systems may be important regulators of gastric function.

Blood flow limitation of stimulated gastric acid secretion in the rat

1986 ◽  
Vol 250 (6) ◽  
pp. G794-G799
Author(s):  
F. W. Leung ◽  
G. L. Kauffman ◽  
J. Washington ◽  
O. U. Scremin ◽  
P. H. Guth
Keyword(s):  
Blood Flow ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Gastric Lavage ◽  
Mucosal Blood Flow ◽  
Hydrogen Gas ◽  
Gastric Acid Output ◽  
Gastric Corpus

Secretagogue-stimulated gastric acid output is reduced when gastric mucosal blood flow is below normal. We tested the hypothesis that the reduction in acid secretion associated with reduced mucosal blood flow was due to a decrease in the delivery of the secretagogue. Gastric acid output was determined by continuous gastric lavage with 0.15 M NaCl, and gastric corpus mucosal blood flow was measured by hydrogen gas clearance in anesthetized, pylorus-ligated rats before and during a period of hypovolemia-induced reduction in mucosal blood flow. A linear correlation between pentagastrin- and histamine-stimulated gastric acid output and gastric corpus mucosal blood flow during hypotension over a range of mucosal blood flow rates was found, and each was expressed as a percentage of the plateau values before hemorrhage. When the dose of pentagastrin was doubled or tripled, or when the stimulation of gastric acid secretion was vagus nerve stimulation, a stimulant of acid secretion that is independent of blood flow for secretatogue delivery, the reduction in gastric acid output by hypotension was not reversed. We conclude that stimulated gastric acid secretion during hemorrhagic hypotension is blood flow-limited and not related to inadequate delivery of secretagogue to parietal cells.

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