Effect of human plasma proteins on stabilisation of platelet anti-aggregatory activity of prostacyclin.
Following the demonstration that biological activity of prostacyclin is more stable in plasma than in buffer solutions at physiological pH, we investigated the possibility that a plasma protein may be responsible for this effect. The duration of platelet anti-aggregatory activity of prostacyclin in fatty acid-free human albumin solution was significantly longer than in buffer solutions. The duration of this 'protection' was proportional to the concentration of albumin; alpha, beta, and gamma-globulin preparations had no 'protective' effect. The degree of 'protection' by albumin solutions was lower than that by plasma despite identical albumin concentrations. This discrepancy may in part be explained by the tendency of plasma to become alkaline on standing, a change that would tend to stabilise prostacyclin. The clinical relevance of our findings is discussed.
D000510:Alpha-Globulins / Q000494:pharmacology; D001609:Beta-Globulins / Q000494:pharmacology; D001798:Blood Proteins / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004355:Drug Stability; D011464:Epoprostenol / Q000494:pharmacology*; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects*; D010976:Platelet Count; D011453:Prostaglandins / Q000494:pharmacology*; D012709:Serum Albumin / Q000494:pharmacology; D005719:gamma-Globulins / Q000494:pharmacology
D000510:Alpha-Globulins; D001609:Beta-Globulins; D001798:Blood Proteins; D011453:Prostaglandins; D012709:Serum Albumin; D005719:gamma-Globulins; D011464:Epoprostenol