Abstract To study the role of the vasodilatory, antiaggregatory prostacyclin (PGI 2) and its endogenous antagonist thromboxane A 2 (TxA 2) in acute pancreatitis, we measured serum thromboxane B 2 (TxB 2, which indicates platelet TxA 2 production) and plasma 6-keto-prostaglandin F 1α (6-keto-PGF 1α, which indicates systemic PGI 2 production) from sequential blood samples in trypsin and taurocholate induced acute canine hemorrhagic pancreatitis (AHP). In addition the effect of a prostaglandin synthesis inhibitor, ibuprofen, was studied and systemic (MAP) and pulmonary artery pressure (MPAP) were recorded for 4.5 hr. The animals were divided into a sham-operated group, an AHP group, an ibuprofen prophylaxis group, and an ibuprofen therapy group. In the sham group the parameters remained stable throughout the experiment. In the AHP group MAP decreased steadily and 6-keto-PGF 1α rose significantly from 80.0 ± 7.8 to 956.0 ± 287.0 pg/ml ( P < 0.001), whereas serum TxB 2 and MPAP remained unchanged. Ibuprofen prophylaxis eliminated the initial fall in MAP and the rise of 6-keto-PGF 1α. Ibuprofen therapy normalized the initially decreased MAP and depressed the level of 6-keto-PGF 1α. We conclude that PGI 2 may at least partly mediate the initial hypotension in canine AHP, whereas platelet TxA 2 production obviously has a negligible role in the development of hemodynamic changes in AHP.