Increased prostacyclin and thromboxane production in man during cardiopulmonary bypass.

To study the effect of the cardiopulmonary bypass (CPB) on the productions of antiaggregatory prostacyclin (PGI2) and proaggregatory thromboxane A2 (TxA2), we collected serial plasma samples from seven patients before, during, and after CPB and assayed them for 6-keto-PGF 1 alpha and thromboxane B2, the main metabolites of PGI2 and TxA2, respectively. The PGI2 production rose significantly (p less than 0.05) following cannulation of the large vessels and remained elevated during the CPB. After discontinuation of CPB, the PGI2 decreased progressively. The TxB2 production also rose during CPB, but later than the increase in PGI2. There was a significant correlation between 6-keto-PGF 1 alpha and TxB2 levels (r = 0.429, p less than 0.001, n = 77). Thus the deficient PGI2 production, or an imbalance between PGI2 and TxA2, does not seem to be responsible for the platelet loss during CPB. By contrast, the human body appears to be protected from platelet aggregation by a surge in endogenous PGI2 during CPB.