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. Author manuscript; available in PMC: 2012 Mar 1.
Published in final edited form as: J Thromb Haemost. 2011 Mar;9(3):531–539. doi: 10.1111/j.1538-7836.2010.04167.x

Fig. 2.

Fig. 2

A comparison between AT and PAI-1 inhibition of TF-FVIIa. FVIIa (10 nM) and relipidated TF (50 nM) were incubated with AT or PAI-1 (1 μM) (panels A and B) in the absence of their cofactors (panel A) or presence of the cofactors, heparin (10 U/ml) or vitronectin (1 μM) (panel B). At varying time intervals, an aliquot was removed from the reaction mixture and residual FVIIa activity was determined as described in Fig. 1. (C) FVIIa (10 nM) and relipidated TF (50 nM) were incubated with varying concentrations of AT or PAI-1 (0 to 1 μM) in the absence or presence of heparin (10 U/ml) or vitronectin (1 μM) for 1 h and the residual FVIIa coagulant activity was determined as described in Materials and Methods. Symbols denote, buffer, (□); PAI-1, (○); AT, (◇) in panel A; buffer, (□); AT, (◇); AT + heparin (◆); PAI-1 + heparin, (▲); PAI-1 + vitronectin, (●) in panels B and C. FVIIa activity measured at 0 min or with no inhibitor was taken as 100%. Data shown in the figure represent mean ± SEM (n=3).