scholarly journals Effects of Exogenous Hydrogen Sulfide in the Hypothalamic Paraventricular Nucleus on Gastric Function in Rats

2022 ◽  
Vol 12 ◽  
Author(s):  
Chenyu Li ◽  
Hongzhao Sun ◽  
Yuan Shi ◽  
Yan Yu ◽  
Xiaofeng Ji ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Paraventricular Nucleus ◽  
Gastric Motility ◽  
Physiological Saline ◽  
Pyrrolidine Dithiocarbamate ◽  
Double Labelling ◽  
Gastric Function

Background: Hydrogen sulfide (H2S) is a new type of gas neurotransmitter discovered in recent years. It plays an important role in various physiological activities. The hypothalamus paraventricular nucleus (PVN) is an important nucleus that regulates gastric function. This study aimed to clarify the role of H2S in the paraventricular nucleus of the hypothalamus on the gastric function of rats.Methods: An immunofluorescence histochemistry double-labelling technique was used to determine whether cystathionine-beta-synthase (CBS) and c-Fos neurons are involved in PVN stress. Through microinjection of different concentrations of NaHS, physiological saline (PS), D-2-Amino-5-phosphonovaleric acid (D-AP5), and pyrrolidine dithiocarbamate (PDTC), we observed gastric motility and gastric acid secretion.Results: c-Fos and CBS co-expressed the most positive neurons after 1 h of restraint and immersion, followed by 3 h, and the least was at 0 h. After injection of different concentrations of NaHS into the PVN, gastric motility and gastric acid secretion in rats were significantly inhibited and promoted, respectively (p < 0.01); however, injection of normal saline, D-AP5, and PDTC did not cause any significant change (p > 0.05). The suppressive effect of NaHS on gastrointestinal motility and the promotional effect of NaHS on gastric acid secretion could be prevented by D-AP5, a specific N-methyl-D-aspartic acid (NMDA) receptor antagonist, and PDTC, an NF-κB inhibitor.Conclusion: There are neurons co-expressing CBS and c-Fos in the PVN, and the injection of NaHS into the PVN can inhibit gastric motility and promote gastric acid secretion in rats. This effect may be mediated by NMDA receptors and the NF-κB signalling pathway.

Gastric motility is a major factor in cold restraint-induced lesion formation in rats

1986 ◽  
Vol 250 (2) ◽  
pp. G191-G199 ◽  
Author(s):  
T. Garrick ◽  
S. Buack ◽  
P. Bass
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Gastric Motility ◽  
Cold Water ◽  
Water Immersion ◽  
High Amplitude ◽  
Cold Water Immersion ◽  
Lesion Formation ◽  
Cold Restraint

These studies were performed to characterize the pattern of gastric contractility associated with cold restraint-induced lesion formation. Gastric motility in the rat was examined with extraluminal transducers at three sites of the stomach. The motility was monitored in the 24-h-fasted state, the postprandial state, and during cold-water immersion restraint. Gastric acid secretion was also monitored in a separate group of animals placed in cold restraint. Both feeding and cold restraint resulted in an equivalent increase in the amplitude of gastric contractions. Prolonged cold restraint, however, resulted in a distinct contractile pattern in which contractions were 56% less frequent and 300-400% longer in duration than those stimulated by feeding. All cold-restrained animals developed multiple gastric erosions. Cold restraint was not associated with increased acid secretion. A single subcutaneous injection of papaverine HCl (50 or 100 mg/kg) suppressed cold restraint-induced high-amplitude contractions and the cold restraint-induced lesion formation without altering acid secretion. These studies suggest that the stimulation of high-amplitude, prolonged duration contractions are more important than changes in gastric acid secretion in the formation of cold restraint-induced gastric lesions.

TRH in dorsal vagal complex mediates acid response to excitation of raphe pallidus neurons in rats

1993 ◽  
Vol 265 (5) ◽  
pp. G880-G886 ◽  
Author(s):  
H. Yang ◽  
G. Ohning ◽  
Y. Tache
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Kainic Acid ◽  
Gastric Fistula ◽  
Dorsal Vagal Complex ◽  
Gastric Function ◽  
Physiological Relevance ◽  
Raphe Pallidus

The role of thyrotropin-releasing hormone (TRH) in the dorsal vagal complex (DVC) in the acid response to excitation of raphe pallidus neurons was investigated in urethan-anesthetized rats with gastric fistula. Kainic acid (0.19 microgram/30 nl) microinjected into the raphe pallidus stimulated gastric acid secretion. The response was prevented by vagotomy. A specific polyclonal TRH antibody, 8964, was raised and characterized (50% inhibitory dose for TRH was 80 pg/ml at an antibody final dilution of 1:10(5)). The TRH antibody injected intracisternally blocked the acid response to intracisternal TRH, but not that of the TRH analogue RX-77368. The TRH antibody (0.33, 0.65, or 1.3 micrograms.100 nl-1.site-1) microinjected bilaterally into the DVC prevented dose dependently by 31, 60, and 76%, respectively, the increase in acid secretion induced by kainic acid injected into the raphe pallidus. The TRH antibody (1.3 microgram/site) microinjected into medullary sites outside of the DVC had no effect. These data indicate that excitation of raphe pallidus neurons induces a vagal-dependent stimulation of gastric acid secretion that is mediated by endogenous TRH in the DVC. TRH neurons in the raphe pallidus projecting to the DVC may have a physiological relevance in the vagal regulation of gastric function.

scholarly journals Effect of simulated intragastric haemorrhage on gastric acid secretion, gastric motility, and serum gastrin.

Gut ◽  
1990 ◽  
Vol 31 (5) ◽  
pp. 518-521 ◽  
Author(s):  
G M Fullarton ◽  
E J Boyd ◽  
G P Crean ◽  
T E Hilditch ◽  
K E McColl
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Gastric Motility ◽  
Serum Gastrin

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.

Fore- and hindbrain mediation of gastric hypoacidity after intracerebral bombesin

1987 ◽  
Vol 252 (5) ◽  
pp. G675-G684 ◽  
Author(s):  
M. W. Gunion ◽  
Y. Tache
Keyword(s):  
Superior Colliculus ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Paraventricular Nucleus ◽  
Ventricular System ◽  
Rat Forebrain ◽  
The Brain ◽  
Bombesin Receptors

Three experiments assessed possible roles of the rat forebrain and hindbrain in the mediation of the gastric hypoacidity induced by intracerebrally administered bombesin. Experiment 1 found that bilateral electrolytic destruction of the paraventricular nucleus of the hypothalamus, which contains numerous bombesin receptors and which is immediately adjacent to the ventricular system, did not alter gastric hypoacidity after intracisternally administered bombesin (500 ng). Experiment 2, done in rats with complete coronal transections of the brain at the superior colliculus, showed that no forebrain structure is absolutely required for intracisternally administered bombesin (0, 30, 100, or 300 ng) to inhibit gastric acid secretion. Experiment 3 determined that bombesin infusions (500 ng) restricted to either the forebrain or the hindbrain by aqueductal plugs are equally effective in inhibiting acid secretion. In sum, these data suggest that both forebrain and hindbrain mechanisms exist that can mediate the inhibition of acid secretion by intracranially administered bombesin; the hindbrain mechanism does not require the forebrain to produce its effect; and lesions of forebrain structures cannot be expected to block bombesin-induced hypoacidity if bombesin reaches the hindbrain.

Interleukin-1 beta acts at hypothalamic sites to inhibit gastric acid secretion in rats

1992 ◽  
Vol 263 (3) ◽  
pp. G414-G418 ◽  
Author(s):  
E. Saperas ◽  
H. Yang ◽  
Y. Tache
Keyword(s):  
Prostaglandin E2 ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Paraventricular Nucleus ◽  
Preoptic Area ◽  
Interleukin 1 ◽  
Medial Preoptic Area ◽  
Anterior Hypothalamus ◽  
Interleukin 1 Beta

It has been established that interleukin-1 beta (IL-1 beta) injected into the cerebrospinal fluid inhibits gastric acid secretion in rats. Brain sites of action of IL-1 beta were investigated in conscious rats implanted unilaterally with chronic hypothalamic cannula. Gastric acid secretion was monitored 2 h after pylorus ligation. Human recombinant IL-1 beta (10 ng) microinjected into the medial preoptic area, anterior hypothalamus, and paraventricular nucleus inhibited gastric acid secretion by 76-83%. IL-1 beta microinjected into the ventromedial hypothalamus and other hypothalamic sites outside of responsive sites had no effect. IL-1 beta inhibitory action in the medial preoptic area was dose related (0.1-10 ng), prevented by indomethacin (5 mg/kg ip), and mimicked by prostaglandin E2. These results show that IL-1 beta acts in the medial preoptic area/anterior hypothalamus and paraventricular nucleus to inhibit acid secretion in pylorus-ligated rats and that IL-1 beta action is likely to involve prostaglandin E2.

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