The Acceleration of Thrombus Formation by Certain Fatty Acids*

Polyunsaturated fatty acids, hyperlipidemia, and thrombosis.

“…In these experiments, long-chain saturated fatty acids such as stearic acid (C18:0) greatly shortened the "thrombus formation time," while polyunsaturated fatty acids were essentially inactive. 9 ' 10 Similarly, intravenous infusions of saturated fatty acids into dogs led to thromboses in the heart and great vessels whereas long-chain polyunsaturated fatty acids such as linoleic acid were much less thrombogenjc11, 108,109 These experiments demonstrated the thrombogenic potential of saturated free fatty acids but it was not yet clear whether they acted via the generation of fibrin (perhaps through activation of factor 12) or whether they also possessed the ability to directly aggregate platelets. Accordingly, experiments were performed with platelets and fatty acids in the absence of plasma coagulation factors.…”

Massive Thrombosis Produced by Fatty Acid Infusion*

“…In this study, two substances believed to activate the Hageman factor did, in fact, cause thrombosis when given intravenously. These were the long-chain, saturated fatty acids and bentonite (7). If Hageman factor activation was the mechanism of the thrombotic effect from the long-chain, saturated fatty acid, it would be suspected that the blood clotting tests reflecting active Hageman factor would be altered.…”

The lipid-chemical features of the metastatic tissues into the liver from the human gastric cancer, large intestinal cancer and malignant insulinoma.

“…This phenomenon could be also explained from the same stand point, because a poly unsaturated fatty acid of cellular phospholipid would increase the fluidity of the cellular membrane as suggested by Horwitz et al (1974). An increase of C18:0 in the percentage value of the phospholipid fatty acid composition of the metastatic lesion of malignant insulinoma may be related to the fact that stearic acid accelerates the blood coagulation reaction (Stuber and Heim 1916;Connor 1962). Considering the occurrence of those differences between primary and metastatic lesions mentioned above, there may be at least two mechanisms to explain those phenomena.…”