Free fatty acidemia as an inducer of systemic hyperfibrinogenemia and fibrinolytic inhibition.
Many major inflammatory stimuli induce secondary conditions of blood hyperfibrinogenemia and fibrinolytic inhibition, changes which may be mediated by alterations in free fatty acid (FFA) metabolism. The effect of a free fatty acidemia induced by the intravenous infusion of a triglyceride into rabbits on the fibrinogen/fibrinolytic system was determined. A 3-h infusion of synthetic fat emulsion induced a rapid rise in FFA (0.4-2.1 microEq/ml in 3 h) followed by a more gradual rise in fibrinogen (2.6-4.3 mg/ml at 24 h), alpha 1-antitrypsin (1.1-1.9 mg/ml at 48 h), and serum fibrinolysis inhibitory activity (increased 202% at 48 h). Increases in protein concentration were due to increased synthesis. It is proposed that the changes in the fibrinogen/fibrinolytic system which follow major inflammatory stimuli are induced by a mediating free fatty acidemia. Possible pharmacological procedures to block these changes are discussed.
D000818:Animals; D001798:Blood Proteins / Q000096:biosynthesis; D005230:Fatty Acids, Nonesterified / Q000097:blood*; D005340:Fibrinogen / Q000378:metabolism*; D005342:Fibrinolysis / Q000187:drug effects*; D006168:Guinea Pigs; D011817:Rabbits; D012709:Serum Albumin; D013997:Time Factors; D014304:Triolein / Q000494:pharmacology; D000515:alpha 1-Antitrypsin
D001798:Blood Proteins; D005230:Fatty Acids, Nonesterified; D012709:Serum Albumin; D000515:alpha 1-Antitrypsin; D014304:Triolein; D005340:Fibrinogen