Key result
Fatty acid sodium salts trigger irreversible platelet aggregation in vitro, with stearate showing highest potency.
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Shows that saturated and unsaturated fatty acids induce irreversible human platelet aggregation, highlighting distinct thrombogenic mechanisms via platelets and clotting factor activation.
The sodium salts of stearic, oleic, linoleic and linolenic acids were added to human washed platelet suspensions and platelet-rich citrated plasma. Aggregation of the platelets was measured microscopically and with a turbidimetric method. All of the fatty acids had the ability to produce aggregation when added to washed platelets, but stearic acid, a long-chain saturated fatty acid, was more potent than were the unsaturated acids when added to platelet-rich plasma. Aggregation of platelets by fatty acids required the presence of calcium ions and the aggregation was irreversible. The addition of albumin diminished the aggregating effects of fatty acids, but microscopic aggregates still formed in most instances. Subnormal aggregation was noted when sodium stearate was added to platelet-rich plasma from a patient with a severe deficiency of factor XII (Hageman factor). Thus, fatty acids are now known to have two potential thrombogenic effects: platelet aggregation and the activation of clotting factors involved in the early stages of blood coagulation.
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Hook et al. (1967) studied Thrombosis and severe factor XII deficiency. Sodium salts of stearic, oleic, linoleic, and linolenic acids vs. Unsaturated fatty acids vs. stearic acid, and addition of albumin was evaluated on Platelet aggregation measured microscopically and with a turbidimetric method. Sodium salts of fatty acids induced irreversible, calcium-dependent human platelet aggregation in vitro, with stearic acid proving more potent than unsaturated fatty acids in platelet-rich plasma.
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