The effect of oxygen radicals on superior mesenteric artery (SMA) blood flow and splanchnic prostaglandin release was examined during early hemorrhage/reperfusion injury. Sprague-Dawley rats were hemorrhaged to 30 mm Hg for 5, 10, or 15 min without (SK5, SK10, and SK15) or with (SK10+R, and SK15+R) blood reperfusion. The SK15+R group were treated with or without superoxide dismutase (SOD 10 000 units/kg intravenously). In vivo SMA blood flow was measured continuously for 100 min by a transonic flow probe. The in vitro-perfused superior mesenteric artery and end organ intestine (SV+SI) were assayed for release of 6-keto-PGF1 alpha, thromboxane B2 (TXB2) and PGE2 by radioimmunoassay. Acute hemorrhage for 10 and 15 minutes increased SV+SI 6-keto-PGF1 alpha release 2-fold and 10-fold respectively compared to the sham (p < 0.01), which was abolished by blood reperfusion. SMA blood flow was decreased by 4% and 60% in the SK10+R and SK15+R groups respectively compared with the sham (p < 0.01). SOD treatment restored both SV+SI release of 6-keto-PGF1 alpha and SMA blood flow to control levels in the SK10+R and SK15+R groups. Oxygen-derived free radicals produced within 15 min of acute hemorrhage/reperfusion injury inhibited splanchnic PGI2 synthesis, which contributed to decreased splanchnic blood flow.