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The effects of albumin bound fatty acids on the platelet inhibitory function of human endothelial cells
Author(s) -
NORDØY ARNE,
SVENSSON BIRGIT,
HOAK JOHN C.
Publication year - 1979
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1979.tb01661.x
Subject(s) - prostacyclin , arachidonic acid , platelet , albumin , biochemistry , chemistry , fatty acid , endothelial stem cell , incubation , prostaglandin , enzyme , in vitro , biology , immunology
. This study was carried out to evaluate the effects of albumin‐bound fatty acids on the anti‐platelet effects of endothelial cells. Primary cultures of human endothelial cells (ECM), grown in confluent monolayers, were incubated with plasma or growth medium enriched with albumin‐bound fatty acids (FA) for 2–20 h. The effects of ECM on ADP‐induced platelet aggregation (PA) and collagen‐induced PA and prostaglandin synthesis in platelet‐rich plasma were tested. ECM released an inhibitor of platelet reactions which resembled the activity of PGI 2 (prostacyclin). The inhibitory activity was increased by preincubation of ECM with arachidonic acid (AA). A moderate decrease of the activity was obtained by incubation with longchain saturated, monoenoic and dienoic unsaturated fatty acids. A pronounced decrease of the inhibitor was obtained by incubation with di‐homo‐γ‐linolenic acid (DHLA). Paired combinations of AA with the other fatty acids in the incubation medium partially restored the inhibitor activity obtained by the separate FA. The stimulation of the inhibitor by AA was dose dependent and high concentrations of AA reduced this activity. The present study indicates that the quantity and quality of the plasma free fatty acids can affect the endothelial cells' ability to act as a non‐thrombogenic surface.