Tumor Necrosis Factor/Cachectin and the Modulation of Endothelial Cell Coagulant Properties
The coagulation mechanism is an effector system capable of rapidly and effectively responding to environmental stimuli. In order to play an integral role in the host response in pathophysiologic states, function of the coagulation mechanism must be linked to the host defense. Since the coagulation mechanism is regulated by tonically active, opposing anticoagulant and procoagulant mechanisms, this suggested the following hypothesis: in homeostasis the balance of coagulation mechanisms on the endothelial cell surface should favor anticoagulation, whereas in stimulated states procoagulant activities would predominate. Sepsis, a disease state with multiple abnormalities of intravascular coagulation, provided an opportunity to test this hypothesis. Our question concerned whether a central mediator of the septic state (1,2), Tumor Necrosis Factor/Cachectin (TNF), could induce the coordinate induction of endothelial cell pro-coagulant activity and suppression of anticoagulant mechanism.
KeywordsAttenuation Thrombin Fibrinogen Auger Fenton
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