Thromb Haemost 1985; 54(02): 418-421
DOI: 10.1055/s-0038-1657863
Original Article
Schattauer GmbH Stuttgart

Reduced Prostacyclin Survival After Fasting-Induced Elevation of Plasma Free Fatty Acids

S H Goodnight
The Division of Hematology and Medical Oncology and Section of Nutrition, Department of Medicine, Oregon Health Sciences University, Portland, Oregon, USA
,
S B Inkeles
The Division of Hematology and Medical Oncology and Section of Nutrition, Department of Medicine, Oregon Health Sciences University, Portland, Oregon, USA
,
N L Kovach
The Division of Hematology and Medical Oncology and Section of Nutrition, Department of Medicine, Oregon Health Sciences University, Portland, Oregon, USA
,
W E Connor
The Division of Hematology and Medical Oncology and Section of Nutrition, Department of Medicine, Oregon Health Sciences University, Portland, Oregon, USA
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Publikationsverlauf

Received 14. Januar 1985

Accepted 25. April 1985

Publikationsdatum:
18. Juli 2018 (online)

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Summary

The anti-thrombotic effect of prostacyclin (PGI2) may be determined not only by its synthetic rate but also by its subsequent survival in blood. After its release from the vascular wall, prostacyclin binds to plasma albumin which stabilizes the molecule and prolongs its inhibitory effects on platelets. In vitro studies have shown that free fatty acids compete for the same albumin binding sites and may therefore displace PGI2 and substantially shorten its survival. To see if this competition could also occur in vivo, we produced a three-fold rise of plasma free fatty acid concentrations in ten normal volunteers by four days of fasting, which led to a significant reduction in prostacyclin survival as measured by a functional assay based on inhibition of ADP-induced platelet aggregation. The shortening of prostacyclin survival was associated with evidence of increased platelet reactivity as measured by the circulating platelet aggregate ratio test. Diseases that produce marked elevations of free fatty acids such as acute myocardial infarction may also lead to shortened PGI2 survival with potentiation of platelet mediated thrombosis.