The effect of hemorrhagic shock on rat splanchnic prostanoid synthesis was examined in vitro. Male rats were bled to a mean pressure of 30 mm Hg for 30 min. At that time a midline laparotomy was performed and the superior mesenteric artery (SMA) was cannulated and removed in continuity with its end organ (SV + SI). The SV + SI was perfused at 3 ml/min with oxygenated Krebs-Henseleit buffer at 37 degrees C. Venous effluent (3 ml) was collected at 15, 30, 60, 90, 120, 150, and 180 min and frozen for analysis of basal prostanoid release. Levels of 6-keto-PGF1 alpha (6-keto), PGE2, thromboxane B2 (TxB2), and PGF2 alpha were analyzed by radioimmunoassay and compared in the shock (SK) and sham-operated control (SM) animals. SK 6-keto and TxB2 increased significantly at 15 min of perfusion and then decreased to a lower baseline from 60 through 120 min of perfusion. The major prostanoid released at all time periods was 6-keto (2 to 20 times higher than other prostanoids). One-way ANOVA (pooled times) showed that 6-keto significantly increased in the SK group compared to the SM group (P less than 0.02). These data suggest that the splanchnic bed attempts to compensate for hemorrhagic shock by the marked release of the endogenous vasodilator prostacyclin. Release of the other prostanoids (including TxB2) from the splanchnic bed was modest in our model.