Alcohol injury to gastric mucosa in mice and its potentiation by stress.

This investigation was initiated to separately evaluate the roles of dose and concentration of ethanol ingestion in the development of acute gastric mucosal injury and to determine the significance of stress as a potentiating factor in ethanol damage. A total of 423 mice were used in this study. Alcohol at the low concentration of 10% and at any of the doses used (1-5 g/kh wt) did not cause gastric mucosal lesions. Similarly, alcohol at the low dose of 1 g/kg wt at any of the concentrations used (10-50%) did not produce any gross injury to the stomach. A single oral administration of ethanol, given at doses of 2-5 g/kg wt and at concentrations of 25-50%, resulted in hyperemia and multiple fundic erosions and, less frequently, antral erosion. The incidence, number, and severity of these lesions rapidly increased with increase in ethanol concentration, ethanol dose, or both. Healing was rapid; at best, lesions were only barely visible 72 hours after alcohol ingestion. Repeated daily doses of ethanol given for 3-5 days did not increase the incidence and number of lesions, probably due to their capacity for rapid healing. Mild stress, in the form of 1-hour restraint in the cold room at 8 degrees C, by itself caused very little mucosal injury in mice, but significantly potentiated the injurious effect of 35% ethanol administered in a 3 g/kh dose. Stress following alcohol intake potentiated gastric mucosal injury much more than if the stress preceded the alcohol ingestion. The incidence, number, and severity of erosions was here 3,4 and 11 times, respectively, greater than the additive effect of alcohol and stress together (P smaller than 0.001). Thus, the extent of ethanol damage to the stomach related both to the concentration and dose of ethanol infested. Stress, especially when following excessive ethanol intake, was a highly significant factor in the potentiation of acute alcoholic gastric mucosal injury.