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游离脂肪酸血症作为系统性高纤维蛋白原血症和纤溶抑制的诱导因素。

Free fatty acidemia as an inducer of systemic hyperfibrinogenemia and fibrinolytic inhibition.

作者信息

Pickart L

出版信息

Inflammation. 1981 Mar;5(1):61-70. doi: 10.1007/BF00910780.

Abstract

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.

摘要

许多主要的炎症刺激会引发继发性血纤维蛋白原血症和纤溶抑制状态,这些变化可能由游离脂肪酸(FFA)代谢的改变介导。研究了通过向兔子静脉输注甘油三酯诱导的游离脂肪酸血症对纤维蛋白原/纤溶系统的影响。输注3小时的合成脂肪乳剂导致FFA迅速升高(3小时内从0.4微当量/毫升升至2.1微当量/毫升),随后纤维蛋白原逐渐升高(24小时时为2.6至4.3毫克/毫升)、α1-抗胰蛋白酶升高(48小时时为1.1至1.9毫克/毫升)以及血清纤溶抑制活性升高(48小时时增加202%)。蛋白质浓度的增加是由于合成增加所致。有人提出,主要炎症刺激后纤维蛋白原/纤溶系统的变化是由介导的游离脂肪酸血症引起的。文中还讨论了阻断这些变化的可能药理学方法。

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