Protection of prostacyclin-like activity in human plasma-a non-enzymatic mechanism?
1. The rate of decay of the platelet antiaggregatory activity of prostacyclin in plasma and buffer solutions was investigated. 2. Platelet anti-aggregatory activity of prostacyclin was more stable in plasma than in buffer solutions at physiological pH. 3. The rate of decay of this activity increased with an increase in incubation temperature. 4. Preheating of plasma at 65 degrees C led to a marked but not total loss of its ability to "protect" prostacyclin. 5. Incubation of 6-keto prostaglandin F 1 alpha in plasma did not result in the appearance of platelet anti-aggregatory activity; nor did the decay curves of prostacyclin activity indicate the emergence of any new platelet anti-aggregatory activity. 6. Incubation of 6-keto-prostaglandin E1 in plasma did not lead to any loss of its platelet anti-aggregatory activity for prolonged periods. 7. We conclude that the marked prolongation of platelet anti-aggregatory activity of prostacyclin in plasma is not due to its enzymatic conversion into 6-keto-prostaglandin E1 but due to 'protection' of prostacyclin itself. This 'protection' is probably due to an interaction with a plasma protein.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000527:Alprostadil / Q000031:analogs & derivatives*; D011464:Epoprostenol / Q000097:blood*; D006358:Hot Temperature; D006801:Humans; D010974:Platelet Aggregation; D011453:Prostaglandins / Q000097:blood*; D011458:Prostaglandins E / Q000097:blood; D013997:Time Factors
D011453:Prostaglandins; D011458:Prostaglandins E; D015121:6-Ketoprostaglandin F1 alpha; C022950:6-ketoprostaglandin E1; D011464:Epoprostenol; D000527:Alprostadil