The Vagus Nerve and its Non-cholinergic Mechanism in the Modulation of Ethanol-induced Gastric Mucosal Damage in Rats

Abstract

The role of the cholinergic pathway in the vagus nerve in modulating gastric lesion formation by ethanol was examined, using an ex-vivo stomach chamber preparation. Subdiaphragmatic vagotomy significantly increased the lesion areas but lowered acid secretion and gastric mucosal blood flow (GMBF). Atropine had no effect, whereas pirenzepine antagonized ethanol-induced mucosal damage. All three procedures showed similar potencies in depressing acid secretion, but only pirenzepine reversed the fall in the GMBF produced by ethanol. These differential effects of vagotomy, atropine and pirenzepine on gastric function suggest that the cholinergic component in the vagus nerve may not be important in the formation of ethanol-induced gastric damage. The persistent protective action as well as the restoration of ethanol-induced GMBF drop by pirenzepine in vagotomized animals further support this hypothesis. The worsening effect of vagotomy is probably modulated by a non-cholinergic mechanism, the abolition of which makes the gastric mucosa more susceptible to damage by ethanol. The acid-independent protective action of pirenzepine and its influence on the GMBF, which were not exhibited by atropine, are indeed unique and perhaps may be attributed to this non-cholinergic pathway.

Antioxidant Mechanism is Involved in the Gastroprotective Effects of Ozonized Sunflower Oil in Ethanol-Induced Ulcers in Rats

“…Oral administration of absolute ethanol in rats is noxious for the stomach, affecting the gastric mucosa topically by disrupting its barrier and provoking pronounced microvascular changes in few minutes after its application. Thus, rapid and strong vasoconstriction is accompanied by rapid and vigorous arteriolar dilation and this combination of microvascular events induces damage in mucosal capillaries [22, 23]. Currently, there is consensus that the former deleterious effects of ethanol on gastric mucosa are consequence of enhanced lipid peroxidation and decreased glutathione (GSH) levels.…”

Investigation of the Mechanisms Underlying the Gastroprotective Effect of Cymbopogon Citratus Essential Oil

“…Thus, rapid and strong vasoconstriction is accompanied by rapid and vigorous arteriolar dilation, and this combination of microvascular events induces damage in mucosal capillaries. [23] Pathophysiology of ulcer is due to an imbalance between aggressive factors (acid, pepsin, Helicobacter pylori , and non-steroidal anti-inflammatory agents) and local mucosal defensive factors (mucus bicarbonate, blood flow, and prostaglandins). [4] The lipid peroxidation mediated by reactive oxygen species is an important cause of destruction and damage to cell membranes, and it is involved in the pathogenesis of acute mucosal injury induced by ethanol, ischemia-reperfusion, and indomethacin.…”

Sphincter of Oddi function in the Australian brush‐tailed possum is inhibited by intragastric ethanol

“…Numerous investigators have demonstrated that the high doses of IG ethanol induce gastric mucosal damage in rats e.g. [31][32][33][34][43][44][45] We undertook limited gross and microscopic examination of the gastric mucosa from several possums that received the 3 g kg )1 IG ethanol and noted some haemorrhage and mucosal oedema (data not presented). This prompted us to consider a possible role for gastric mucosal damage in the ethanol-induced fall in TSF.…”