The role of active oxygen species in the pathogenesis of intestinal mucosal damage was investigated in a rat model produced by hemorrhagic shock. After the treatment of ischemia-reperfusion, intestinal mucosal damage was observed in jejunum and ileum. Intestinal mucosal blood flow and superoxide dismutase (SOD) activity decrease in jejunum and ileum. Treatment of allopurinol, SOD and antibiotics inhibited intestinal mucosal demage after reperfusion. After reperfusion of fresh blood withdrawn by other rat, in exchange for shedblood, intestinal mucosal lesions were reduced. These results suggest that active oxygen species may be involved in the pathogenesis of hemorrhagic shock induced small intestinal mucosal damage in association with intestinal mucosal blood flow, endtoxin of intestinal bacteriaand other factors in withdrawn blood.