Fr283 THE EFFECT TO THE GASTRIC EMPTYING BY INHIBITING GASTRIC ACID SECRETION

2021 ◽  
Vol 160 (6) ◽  
pp. S-284
Author(s):  
Kazuhiro Ota ◽  
Shinya Nishida ◽  
Toshihisa Takeuchi ◽  
Hideki Tawa ◽  
Taro Iwatsubo ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid

CNS regulation of gastric and autonomic functions in dogs by gastrin-releasing peptide

1988 ◽  
Vol 255 (3) ◽  
pp. G298-G303
Author(s):  
H. J. Lenz
Keyword(s):  
Nervous System ◽  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Left Gastric Artery ◽  
Gastric Artery ◽  
Ganglionic Blockade ◽  
The Central Nervous System ◽  
Artery Flow

The central nervous system effects of canine gastrin-releasing peptide (GRP) were studied on gastric acid secretion, emptying, blood flow, and the autonomic nervous system in conscious dogs. GRP injected into the third cerebral ventricle significantly (P less than 0.01) increased plasma epinephrine but not norepinephrine concentrations. GRP (0.1-1.0 nmol/kg) significantly decreased gastric acid secretion stimulated by an 8% peptone meal, delayed gastric emptying of the liquid peptone meal, and increased left gastric artery flow. Ganglionic blockade, truncal vagotomy, or adrenalectomy did not abolish the inhibitory effect of GRP on gastric acid secretion. However, ganglionic blockade or vagotomy abolished the GRP-induced inhibition of gastric emptying, and ganglionic blockade or adrenalectomy abolished the GRP-induced increases in left gastric artery flow and plasma epinephrine concentrations. An intravenous infusion of epinephrine that produced similar plasma concentrations of epinephrine that were observed after cerebroventricular injection of GRP mimicked the increase in left gastric artery flow induced by GRP. It is concluded that 1) GRP acts within the central nervous system to activate the sympathoadrenal axis, 2) GRP inhibits gastric emptying of a liquid meal by a vagally dependent mechanism and enhances left gastric artery flow by the release of epinephrine from the adrenal medulla, and 3) the pathway(s) that mediate the GRP-induced inhibition of gastric acid in the dog remain unknown.

Gastric acid secretion and gastric emptying of liquids in 99 male duodenal ulcer patients

1989 ◽  
Vol 34 (2) ◽  
pp. 251-256 ◽  
Author(s):  
Roberto Corinaldesi ◽  
Vincenzo Stanghellini ◽  
Giovanni Francesco Paparo ◽  
Anna Paternic� ◽  
Anna Giulia Rusticali ◽  
...  
Keyword(s):  
Duodenal Ulcer ◽  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid

scholarly journals Intestinal fat-induced inhibition of meal-stimulated gastric acid secretion depends on CCK but not peptide YY

1999 ◽  
Vol 276 (2) ◽  
pp. G550-G555 ◽  
Author(s):  
Xiao-Tuan Zhao ◽  
John H. Walsh ◽  
Helen Wong ◽  
Lijie Wang ◽  
Henry C. Lin
Keyword(s):  
Small Intestine ◽  
Gastric Emptying ◽  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Peptide Yy ◽  
Inhibitory Effect ◽  
Proximal Half

Fat in small intestine decreases meal-stimulated gastric acid secretion and slows gastric emptying. CCK is a mediator of this inhibitory effect (an enterogastrone). Because intravenously administered peptide YY (PYY) inhibits acid secretion, endogenous PYY released by fat may also be an enterogastrone. Four dogs were equipped with gastric, duodenal, and midgut fistulas. PYY antibody (anti-PYY) at a dose of 0.5 mg/kg or CCK-A receptor antagonist (devazepide) at a dose of 0.1 mg/kg was administered alone or in combination 10 min before the proximal half of the gut was perfused with 60 mM oleate or buffer. Acid secretion and gastric emptying were measured. We found that 1) peptone-induced gastric acid secretion was inhibited by intestinal fat ( P < 0.0001), 2) inhibition of acid secretion by intestinal fat was reversed by CCK-A receptor antagonist ( P < 0.0001) but not by anti-PYY, and 3) slowing of gastric emptying by fat was reversed by CCK-A antagonist ( P< 0.05) but not by anti-PYY. We concluded that inhibition of peptone meal-induced gastric acid secretion and slowing of gastric emptying by intestinal fat depended on CCK but not on circulating PYY.

Inhibitory effect of intragastric glucose on gastric acid secretion and gastric emptying of liquids in man

1983 ◽  
Vol 28 (6) ◽  
pp. 502-506 ◽  
Author(s):  
Haruka Sasaki ◽  
Murugasu Nagulesparan ◽  
Andre Dubois ◽  
Barbara Vasquez ◽  
Eugene Straus ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Effect

scholarly journals Cocaine-Amphetamine-Regulated Transcript (CART) Acts in the Central Nervous System to Inhibit Gastric Acid Secretion via Brain Corticotropin-Releasing Factor System*

Endocrinology ◽  
2000 ◽  
Vol 141 (8) ◽  
pp. 2854-2860 ◽  
Author(s):  
Toshikatsu Okumura ◽  
Hiroto Yamada ◽  
Wataru Motomura ◽  
Yutaka Kohgo
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Inhibition ◽  
Gastric Function ◽  
The Central Nervous System ◽  
The Brain

Recent study has indicated that cocaine-amphetamine-regulated transcript (CART) is an anorectic chemical in the brain. In the present study, we examined the hypothesis that CART may act in the central nervous system to alter gastric function. Food consumption, gastric acid secretion, and gastric emptying were measured after injection of CART into the cerebrospinal fluid in 24-h fasted Sprague Dawley rats. Central injection of CART inhibited food intake, gastric acid secretion, and gastric emptying. In contrast, ip injection of CART failed to inhibit gastric acid secretion and gastric emptying, suggesting that CART acts in the brain to suppress gastric acid secretion and gastric emptying. In the vagotomized animals, centrally administered CART did inhibit pentagastrin-stimulated gastric acid secretion. The CART-induced acid inhibition was also observed in rats treated with indomethacin, a cyclooxygenase inhibitor. In contrast, pretreatment with central administration of a CRF receptor antagonist,α -helical CRF9–41, completely blocked the central CART-induced inhibition of gastric acid secretion. All these results suggest that CART acts in the brain to inhibit gastric function via brain CRF system. The vagal pathway and the prostaglandin system are not involved in the acid inhibition.

Targeted disruption of the murine CCK1 receptor gene reduces intestinal lipid-induced feedback inhibition of gastric function

2006 ◽  
Vol 291 (1) ◽  
pp. G156-G162 ◽  
Author(s):  
K. L. Whited ◽  
D. Thao ◽  
K. C. Kent Lloyd ◽  
A. S. Kopin ◽  
H. E. Raybould
Keyword(s):  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Feedback Inhibition ◽  
Vagal Afferents ◽  
Afferent Pathway ◽  
Gastric Function ◽  
Vagal Afferent ◽  
Fos Expression

Cholecystokinin (CCK), acting at CCK1 receptors (CCK1Rs) on intestinal vagal afferent terminals, has been implicated in the control of gastrointestinal function and food intake. Using CCK1R−/− mice, we tested the hypothesis that lipid-induced activation of the vagal afferent pathway and intestinal feedback of gastric function is CCK1R dependent. In anesthetized CCK1R+/+ (“wild type”) mice, meal-stimulated gastric acid secretion was inhibited by intestinal lipid infusion; this was abolished in CCK1R−/− mice. Gastric emptying of whole egg, measured by nuclear scintigraphy in awake mice, was significantly faster in CCK1R−/− than CCK1R+/+ mice. Gastric emptying of chow was significantly slowed in response to administration of CCK-8 (22 pmol) in CCK1R+/+ but not CCK1R−/− mice. Activation of the vagal afferent pathway was measured by immunohistochemical localization of Fos protein in the nucleus of the solitary tract (NTS; a region where vagal afferents terminate). CCK-8 (22 pmol ip) increased neuronal Fos expression in the NTS of fasted CCK1R+/+ mice; CCK-induced Fos expression was reduced by 97% in CCK1R−/− compared with CCK1R+/+ mice. Intralipid (0.2 ml of 20% Intralipid and 0.04 g lipid), but not saline, gavage increased Fos expression in the NTS of fasted CCK1R+/+ mice; lipid-induced Fos expression was decreased by 47% in CCK1R−/− compared with CCK1R+/+mice. We conclude that intestinal lipid activates the vagal afferent pathway, decreases gastric acid secretion, and delays gastric emptying via a CCK1R-dependent mechanism. Thus, despite a relatively normal phenotype, intestinal feedback in response to lipid is severely impaired in these mice.

NERP-2 regulates gastric acid secretion and gastric emptying via the orexin pathway

2017 ◽  
Vol 485 (2) ◽  
pp. 409-413 ◽  
Author(s):  
Cherl Namkoong ◽  
Koji Toshinai ◽  
T.M. Zaved Waise ◽  
Hideyuki Sakoda ◽  
Kazuki Sasaki ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid
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