Route of ethanol administration and gastric acid output during chronic conditions

The effect of intravenous or intragastric ethanol on gastric secretion was determined in chronic ethanol-fed and matched control rats. In vivo, basal and histamine-stimulated acid outputs were inhibited by acute intragastric ethanol to a greater extent in chronic control rats than in ethanol-fed rats. In contrast, intravenous ethanol stimulated basal and potentiated histamine (H)-stimulated acid output (blocked by cimetidine but not atropine) in ethanol-fed rats but not in chronic control rats. Serum gastrin levels were not significantly altered by ethanol. In vitro, mucosal ethanol inhibited basal and H-stimulated acid secretion by mucosae from chronic control and ethanol-fed rats, but serosal ethanol did not significantly alter acid secretion. In conclusion, chronic ethanol intake results in higher acid outputs following acute exposure to intravenous or intragastric ethanol or in vitro exposure to mucosal ethanol as compared to studies using matched control rats.