Coagulation proteases increase inflammation during endotoxemia via PARs. FVIIa and FXa activation of PAR-2 and thrombin (IIa) activation of PAR-1 and PAR-4 may enhance inflammation. Thrombin also cleaves fibrinogen to fibrin and activates platelets by cleavage of PAR-3/4. Inhibitors of the TF-FVIIa complex are shown: αTF Ab (anti-TF antibody), FVIIai (active site-inhibited FVIIa), and TFPI-1. Hirudin inhibits thrombin, and ancrod depletes fibrinogen.