scholarly journals Intracerebroventricularly Administered Nicotine Inhibits Vagally Stimulated Gastric Acid Output in Rats by Activating the Central Sympatho-Adrenal Outflow

1987 ◽  
Vol 45 (2) ◽  
pp. 288-291
Author(s):  
Kunihiko YOKOTANI ◽  
Yasunobu OKUMA ◽  
Yoshitsugu OSUMI
Keyword(s):  
Gastric Acid ◽  
Acid Output ◽  
Gastric Acid Output

scholarly journals PAC1 Deficiency in a Murine Model Induces Gastric Mucosa Hypertrophy and Higher Basal Gastric Acid Output

2010 ◽  
Vol 43 (1) ◽  
pp. 76-84 ◽  
Author(s):  
Yuxin Lu ◽  
Patrizia Germano ◽  
Gordon V. Ohning ◽  
John P. Vu ◽  
Joseph R. Pisegna
Keyword(s):  
Gastric Mucosa ◽  
Gastric Acid ◽  
Murine Model ◽  
Acid Output ◽  
Gastric Acid Output

Effect of vagotomy on the acid response to gastric distension

1970 ◽  
Vol 48 (10) ◽  
pp. 670-674 ◽  
Author(s):  
R. M. Preshaw
Keyword(s):  
Motor Activity ◽  
Gastric Acid ◽  
Motor Response ◽  
Acid Output ◽  
The Body ◽  
Conscious Dogs ◽  
Truncal Vagotomy ◽  
Gastric Distension ◽  
Gastric Acid Output

Distension of the body of the stomach, in conscious dogs with vagally innervated antral pouches, caused an increase in gastric acid output, and an increase in antral motor activity. Truncal vagotomy inhibited the acid response to distension, but had no effect on the antral motor response. Denervation of the antral pouch by separating it from the main stomach caused little further diminution in the response.

scholarly journals A new method for determining gastric acid output using a wireless pH-sensing capsule

2013 ◽  
Vol 37 (12) ◽  
pp. 1198-1209 ◽  
Author(s):  
D. H. Weinstein ◽  
S. deRijke ◽  
C. C. Chow ◽  
L. Foruraghi ◽  
X. Zhao ◽  
...  
Keyword(s):  
Gastric Acid ◽  
Acid Output ◽  
New Method ◽  
Ph Sensing ◽  
Gastric Acid Output

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.

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.

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