Recent Advances in the Gastric Mucosal Protection Against Stress-induced Gastric Lesions. Importance of Renin-angiotensin Vasoactive Metabolites, Gaseous Mediators and Appetite Peptides

2017 ◽  
Vol 23 (27) ◽  
Author(s):  
Tomasz Brzozowski ◽  
Katarzyna Magierowska ◽  
Marcin Magierowski ◽  
Agata Ptak-Belowska ◽  
Robert Pajdo ◽  
...  
Keyword(s):  
Mucosal Protection ◽  
Gastric Lesions ◽  
Renin Angiotensin ◽  
Recent Advances ◽  
Gastric Mucosal Protection

Nonprotein sulfhydryl compounds in canine gastric mucosa: effects of PGE2 and ethanol

1985 ◽  
Vol 249 (1) ◽  
pp. G137-G144 ◽  
Author(s):  
T. A. Miller ◽  
D. Li ◽  
Y. J. Kuo ◽  
K. L. Schmidt ◽  
L. L. Shanbour
Keyword(s):  
Gastric Mucosa ◽  
Low Dose ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
High Dose ◽  
Mucosal Protection ◽  
Gastric Mucosal Protection ◽  
Sulfhydryl Compounds ◽  
Mild Irritants

By use of an in vivo canine chambered stomach preparation in which the gastric mucosa was partitioned into two equal halves, the effect of topical 16,16-dimethyl PGE2 (DMPGE2) (1 microgram/ml of perfusate) and 8% and 40% ethanol on tissue levels of nonprotein sulfhydryl compounds was assessed. Both DMPGE2 and 8% ethanol significantly increased (P less than 0.005) mucosal levels of nonprotein sulfhydryls when compared with corresponding mucosa bathed with saline alone. In contrast, mucosa bathed with 40% ethanol showed significantly decreased levels. If mucosa was bathed with DMPGE2 or 8% ethanol prior to exposing the stomach to 40% ethanol, this depletion in sulfhydryl compounds was not observed. Since other experimental observations have shown that exogenously administered prostaglandins and mild irritants (such as low-dose alcohol) can prevent gastric mucosal damage by necrotizing agents (such as high-dose alcohol), our findings are consistent with the hypothesis that nonprotein sulfhydryls may play a role in mediating gastric mucosal protection.

scholarly journals Role of gap junctions in gastric mucosal protection.

1993 ◽  
Vol 61 ◽  
pp. 107
Author(s):  
Fujsao Ueda ◽  
Kiyotaka Mimura ◽  
Shin-ichi Tsuchiya ◽  
Kiyoshi Kimura
Keyword(s):  
Gap Junctions ◽  
Mucosal Protection ◽  
Gastric Mucosal Protection

Mesolimbic dopamine mediates gastric mucosal protection by central neurotensin

1991 ◽  
Vol 260 (1) ◽  
pp. G34-G38 ◽  
Author(s):  
L. P. Xing ◽  
C. Balaban ◽  
J. Seaton ◽  
J. Washington ◽  
G. Kauffman
Keyword(s):  
Nucleus Accumbens ◽  
Substantia Nigra ◽  
Acid Secretion ◽  
Lateral Ventricle ◽  
Cold Water ◽  
Mucosal Injury ◽  
Mucosal Protection ◽  
Minimal Effective Dose ◽  
Gastric Mucosal Protection ◽  
6 Hydroxydopamine

Bilateral microinjection (1.0 microliter/side) of neurotensin (NT; 0.3, 1.5, and 3.0 micrograms/side) into the nucleus accumbens (NACB) and ventral tegmental area (VTA) but not in substantia nigra and striatum reduced gastric mucosal injury produced by 2 h of cold-water restraint (CWR). The minimal effective dose for NT-induced protection was 10-100 times lower when administered directly into NACB than into the lateral ventricle. These effects were blocked by pretreatment with the dopamine (DA) receptor antagonist, haloperidol (Hal; 0.5 microgram/side) given directly into NACB. Injection of 6-hydroxydopamine into VTA depleted endogenous DA and inhibited gastric mucosal protection against CWR-induced injury afforded by NT pretreatment. NT, given into either VTA and NACB, inhibited pentagastrin-stimulated gastric acid secretion. These results suggest that VTA and NACB, which represent the mesolimbic DA system, are important locations for interaction between NT and DA receptors to produce gastric mucosal protection against CWR-induced injury.

Gastric mucosal protection by chronic restraint: effects of vagotomy

1985 ◽  
Vol 248 (1) ◽  
pp. G35-G39 ◽  
Author(s):  
J. L. Wallace ◽  
G. P. Morris ◽  
M. M. Cohen
Keyword(s):  
Gastric Damage ◽  
Gastric Injury ◽  
Surface Epithelium ◽  
Intragastric Administration ◽  
Mucosal Protection ◽  
Previous Exposure ◽  
Vagal Innervation ◽  
Gastric Mucosal Protection ◽  
And Control ◽  
Ethanol Injury

This study was performed to determine the effects of vagotomy on the gastric mucosal resistance to ethanol injury that develops in the rat in response to prolonged mild restraint. The resistance to ethanol injury up to 4 days after cessation of chronic mild restraint (CMR) was also examined. Intragastric administration of ethanol/acid to rats previously subjected to 10 days of CMR produced significantly (P less than 0.0001) less damage than to the mucosae of control rats. While previous exposure to CMR appeared to prevent the necrotic gastric damage induced by ethanol, damage to the surface epithelium was not prevented. When similar experiments were performed on CMR and control rats that had truncal vagotomy, the extent of ethanol/acid injury in the two groups was not significantly different. Intragastric administration of ethanol/acid to 8-day CMR rats produced 91% less (P less than 0.005) gastric damage than in control rats. When ethanol was administered 2 days after cessation of CMR, the gastric injury was still significantly less (P less than 0.01) than in control rats. However, when ethanol was administered 4 days after cessation of CMR, the resulting damage was not significantly different from that of control mucosae. These studies suggest that intact vagal innervation may be necessary for adaptation of the gastric mucosa to chronic mild restraint. These adaptive changes are still present up to 4 days after cessation of the restraint procedure.

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