Abstract
The half-life of the platelet antiaggregatory activity of prostacyclin (PGI 2) is prolonged when PGI 2 is incubated in human plasma or in fatty-acid-free human albumin solutions. This “PGI 2-protective” effect is diminished when fatty acids are added to the incubate, and the diminution is proportional to the concentration of the nonesterified fatty acids added. Unsaturated fatty acids were more potent in causing this reduction than saturated acids. It is possible that nonesterified fatty acids displace PGI 2 from binding sites on the albumin molecule and that they may thus alter the biologic half-life of any circulating PGI 2. This observation may partly account for the well-documented association between reised serum nonesterified fatty acid levels and thrombosis/platelet activation.
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