Laparotomy stimulates an endogenous gastric mucosal protective mechanism in the rat. A microcirculatory and morphologic study of ethanol injury.

In vivo microscopy in the anesthetized rat unexpectedly revealed that the topical application of 75% ethanol to the gastric mucosa had no effect on the mucosal microcirculation. If, however, the synthesis of endogenous prostaglandin was inhibited by indomethacin, the topical application of 75% ethanol resulted in complete superficial mucosal microcirculatory stasis in the majority of rats. In indomethacin-pretreated rats, Rioprostil, a synthetic prostaglandin E1 analogue, reversed this effect of topical ethanol. The degree of ethanol-induced histologic gastric mucosal damage was inversely correlated with time to complete stasis. Ethanol injury studies under various conditions revealed that laparotomy stimulated a gastric protective mechanism that persisted for between 1 and 2 h and that was blocked by indomethacin. In conclusion, (a) laparotomy stimulates a gastric mucosal protective mechanism that probably is mediated by prostaglandin synthesis, and (b) cessation of mucosal blood flow appears to be an important early step in ethanol-induced gastric mucosal injury, and maintenance of mucosal blood flow by endogenous or exogenous prostaglandin may play a major role in prostaglandin protection.