Prostacyclin inhibits 5-hydroxytryptamine release but stimulates thromboxane synthesis during cardiopulmonary bypass

The antiaggregating agent prostacyclin (PGI2) was infused into ten dogs during cardiopulmonary bypass (CPB) to minimize thrombocytopenia and platelet dysfunction. The animals were anesthetized, placed on mechanical ventilation and underwent thoracotomy. After heparinization with 300 u/kg, animals were assigned to control (n=5) or PGI2 treated groups (n=5). Thoracotomy and then CPB decreased platelet numbers to below 30,000/mm3 (p less than 0.05) and fibrinogen to less than 150 mg/dl (p less than 0.05). PGI2 at 100 ng/kg.min was infused for the 2 h period of CPB. PGI2 infusion did not prevent these changes, but did prevent platelet serotonin release. In the control group after CPB, platelet serotonin fell from the baseline value of 1.11 microgram/10(9) to 0.35 microgram/10(9) platelets (p less than 0.05). In contrast, PGI2 treatment resulted in a serotonin increase to 2.27 micrograms/10(9) platelets (p less than 0.05). Thromboxane B2 concentrations of platelets and plasma rose during CPB (p less than 0.05). Surprisingly, PGI2 infusion accentuated this rise in platelet and plasma thromboxane B2 (p less than 0.05). These data indicate that during CPB, an infusion of PGI2: 1) does not prevent thrombocytopenia; 2) increases platelet serotonin uptake despite, 3) an associated rise in platelet and plasma thromboxane B2.