The gastric mucosa is characterized by high rates of surface epithelial cell (SEC) loss. Exposure to acute stressors results in an increase in the incidence of SEC loss. However, little is known about the detachment of SEC from the epithelial sheet. We have used scanning and transmission electron microscopy to study mechanisms of SEC loss from the gastric mucosae of normal, fasted rats and of rats exposed to acute stressors. In fasted control animals SEC loss occurred primarily via extrusion of individual interfoveolar cells and only rarely by degeneration in situ. Each extruding cell was surrounded by a rosette-like configuration of adjacent, encroaching SEC. Mucosal integrity is maintained. Short term exposure to acute stressors results in an increase in the incidence of extrusive cell loss. Continued exposure to stressors also increases the incidence of degeneration in situ of isolated SEC or groups of SEC. Extrusion provides a mechanism for the necessary removal of gastric SEC. Acute stress may override or exhaust the extrusive mode, producing, via ischemia or surface diffusion of cytotoxic agents, SEC degeneration in situ and breaks in the mucosal barrier.