Corpus ID: 46830227

Labile aggregation stimulating substance, free fatty acids, and platelet aggregation.

  title={Labile aggregation stimulating substance, free fatty acids, and platelet aggregation.},
  author={Jonathan M. Gerrard and J. G. White and William Krivit},
  journal={The Journal of laboratory and clinical medicine},
  volume={87 1},
Labile aggregation stimulating substance (LASS), an intermediate produced during platelet biosynthesis of PGE2 and PGF2alpha, acts as a physiologic intercellular messenger to promote platelet aggregation and the release reaction. The activity is formed by intact cells after physiologic stimulation or can be generated from platelet membrane fractions after combination with arachidonate. In the present investigation, small amounts of polyunsaturated fatty acids added to an incubation mixture of… Expand
27 Citations
Enrichment of human platelet phospholipids with linoleic acid diminishes thromboxane release.
Exposure of human platelets to elevated concentrations of linoleic acid, the principal dietary polyunsaturate, would influence platelet thromboxane A2 release was investigated, suggesting that the platelet cyclooxygenase was partially inhibited. Expand
Inhibition of platelet function by cis-unsaturated fatty acids.
In studies of gel-filtered human platelets, it is found that cis-unsaturated fatty acids inhibited platelet shape change, aggregation, and secretion of 5-hydroxytryptamine induced by thrombin, adenosine diphosphate (ADP), collagen, U46619, or plant lectins, but not that induced by A23187, a calcium ionophore. Expand
Inhibition of platelet phospholipase-A2 as a mechanism for the anti-aggregating effect of linoleic acid
The conclusion is made that the anti-aggregating effect of linoleic acid is independent from prostaglandin pathway and is probably related to the phospholipid metabolism. Expand
The chemiluminescence response of human platelets.
These studies implicate activation of the enzyme prostaglandin synthetase in the arachidonate-induced platelet chemiluminescence and provide evidence that linoleic acid may also specifically activate platelet cyclooxygenase to produce electronically excited species capable of light emission. Expand
Effect of fatty acid modification on prostacyclin production by cultured human endothelial cells.
There was a progressive increase in the capacity of the cells to release PGI2 in response to thrombin and the increase correlated with a reduction in linoleate content of the cell lipids, but there was no change in arachidonate content, which suggests that linoleic acid may act as an inhibitor of P GI2 production. Expand
An endogenous inhibitor of PAF-induced platelet aggregation, isolated from rat liver, has been identified as free fatty acid.
In an earlier study, an inhibitor of PAF-induced aggregation of platelets was isolated from perfused rat liver and found to be a mixture of long-chain unsaturated fatty acids, which could have interesting connotations as regards modulation ofPAF activity. Expand
Isomers of trans fatty acids modify the activity of platelet 12-P lipoxygenase and cyclooxygenase/thromboxane synthase.
The effects of fatty acids are demonstrated at the membrane level where fatty acids may produce a perturbation in specific lipid domains affecting the activity of cytoplasmic enzymes like 12-P LOX and cyclooxygenase/thromboxane synthase. Expand
Platelet Fatty Acid Composition and Adenosine Diphosphate-Induced Platelet Aggregation
1) The fatty acid composition (16:0, 18:0, 18:1, 18:2, 20:4 in wt%) of platelet total lipids and platelet aggregation (PAG) in citrated PRP induced by ADP (1 and 0.1mM) were studied in 20 normalExpand
Docosahexaenoic acid (C22:6 omega 3) and linoleic acid are anti-aggregatory, and alter arachidonic acid metabolism in human platelets.
DHA showed a dose-dependent inhibition of platelet aggregation induced by arachidonate, epinephrine and collagen, and this effect was greatest for PGE2 which increased by 5-6 fold of control values. Expand
Effect of dietary linoleic acid on platelet function in the rat.
In rat, dietary linoleic acid is apparently responsible for a specific protective effect on platelet functions which cannot be observed by merely decreasing the level of saturated fat. Expand