Abstract
Abstract Platelet rich plasma (PRP) added albumin bound fatty acids (stearic acid, oleic acid, linoleic acid) (LA), α-linolenic acid, di-homo-γ-`linolenic (DHLA) and arachidonic acid (AA), ratio 2, were preincubated with and without endothelial cell monolayers (ECM), prepared from human umbilical veins, for 90 min at room temperature. Aliquots of PRP were then exposed to ADP and collagen, and platelet aggregation (PA) and malondialdehyde(MDA) production after collagen-induced PA were measured. DHLA inhibited PA in PRP, and in PRP incubated with ECM, whereas LA and AA were inhibitory only after preincubation with ECM. MDA production only partially followed PA. When PRP were incubated with albumin bound FA and then added prostacyclin (PGI2) or 6-keto-PGFlα (20 nmol/1) before exposure to the aggregating agents, PGI2 regularly inhibited PA. Only PRP incubated with DHLA showed a significant less aggregation than PRP incubated with albumin or the other FA. This study shows that the effects of the linoleate sequence of fatty acids on platelets and endothelial cells are different than on platelets in the absence of endothelial cells. This probably reflects the two cell types different ability to convert and metabolize the various FA to platelet activity prostaglandins and thromboxanes, and may be of significance for the influence of albumin bound FA on the thrombosis mechanism.
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