The aim was to study the effect of indometacin (IM) induced gastrointestinal injury on somatic pain sensitivity in awake rats. IM was administered at the ulcerogenic dose (35 mg/kg, s. c.) to fasted (24 h) and fed rats. Somatic pain sensitivity was evaluated using a tail flick test. Latency time was measured under conditions of the formation of gastric erosion (1 - 4 h after IM injection) as well as small intestinal injury (24, 48 and 72 h after IM injection). IM administration caused the gastric erosion formation only in fasted rats (4 h after the administration) and the small intestinal injury in both fasted and fed rats (24, 48, 72 h after the administration). Indomethacin-caused gastric and small intestinal injury resulted in an increase in tail flick latency. We did not observe any changes in tail flick latency in IM-treated rats without significant gastrointestinal injury. The gastrointestinal injury was accompanied by signs of chronic stress: long-lasting increase in corticosterone blood level, adrenal hypertrophy, thymus involution, and loss of body weight. Thus, the IM-induced gastrointestinal injury formation resulted in somatic pain inhibition in awake rats.