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

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.

1985 ◽  
Vol 249 (1) ◽  
pp. G137-G144 ◽  
Author(s):  
T. A. Miller ◽  
D. Li ◽  
Y. J. Kuo ◽  
K. L. Schmidt ◽  
L. L. Shanbour

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.


1993 ◽  
Vol 61 ◽  
pp. 107
Author(s):  
Fujsao Ueda ◽  
Kiyotaka Mimura ◽  
Shin-ichi Tsuchiya ◽  
Kiyoshi Kimura

1991 ◽  
Vol 260 (1) ◽  
pp. G34-G38 ◽  
Author(s):  
L. P. Xing ◽  
C. Balaban ◽  
J. Seaton ◽  
J. Washington ◽  
G. Kauffman

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.


1984 ◽  
Vol 247 (3) ◽  
pp. G296-G304 ◽  
Author(s):  
A. Robert ◽  
D. Eberle ◽  
N. Kaplowitz

Exogenous thiol compounds have been reported to protect the stomach from ethanol-induced necrotic lesions. The gastric mucosa contains high levels of an endogenous thiol, glutathion (GSH). Because of the known role of glutathione in protecting against hepatic injury, its role in gastric mucosal cytoprotection was of interest. By use of an animal model for acute gastric injury from ethanol, a close parallel relation between depletion of endogenous mucosal GSH and induction of mucosal protection was demonstrated. Surprisingly, mucosal protection varied inversely with the level of mucosal GSH obtained after treatment with specific GSH-depleting agents (diethyl maleate and cyclohexene-1-one). Depletion of gastric mucosal GSH was associated with an increase in the mucosal content of prostaglandins 6-keto F1 alpha and F2 alpha but not E2. The protective effect induced by GSH-depleting agents was partially reversed by indomethacin in some but not all studies. Although GSH depletors increased gastric juice volume, protection with these agents persisted after the volume and mucosal GSH had returned to control levels and also was not reversed by increasing the dose of ethanol threefold to overcome a possible dilutional effect. We conclude that, contrary to apparent predictions, depletion of endogenous gastric GSH protects the stomach from acute ethanol-induced injury. Although the mechanism of this protection is unknown, a mediation by endogenous release of prostaglandins seems to play a minor role since diethyl maleate was protective even in indomethacin-treated animals.


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