Aim: 

Ethanol in high concentrations is a known irritant of the gastrointestinal tract. After alcohol ingestion ethanol is absorbed by passive diffusion, the largest fraction in the proximal small intestine. The ethanol exposure can induce both functional and morphological changes in the duodenal mucosa. Duodenal mucosal bicarbonate secretion (DBS) is considered an important mechanism of epithelial defense against discharge from the stomach. Previously, ethanol has been reported to decrease DBS in the rabbit duodenal mucosa mounted in Ussing chamber. In the present study, we examined the mechanism involved in the duodenal secretory response to a moderate dose of ethanol in the rat in vivo.

Methods: 

Rats were anaesthetized and a 30 mm segment of the proximal duodenum with an intact blood supply was perfused in situ with saline or saline containing ethanol (15%, v/v). Effects on DBS and net fluid flux were investigated. Agents were administered luminally, intravenously (i.v.) and/or intraperitonealy (i.p.).

Results: 

Perfusing the duodenal segment with ethanol (15%) for 30-min increases DBS two-fold but does not alter the net fluid flux. Pre-treating the animals with a CFTR inhibitor (CFTRinh172) i.p. or i.v. did not change the secretory response to ethanol. Hexamethonium (i.v.), but not capsazepine (i.v.), reduced the ethanol-induced increase in DBS. Removing Cl? from the luminal perfusate abolished the ethanol-induced increase in DBS whilst the net fluid flux remained unchanged.

Conclusion: 

Ethanol induces increases in DBS by activating epithelial apical Cl^-/HCO3^- exchangers. The duodenal secretory response to ethanol is partly mediated by enteric neural pathways involving nicotinic receptors.