Table 4

Time to carotid artery occlusion with FeCl3-induced injury

GroupGenotype*SampleDose (µg/kg)No. of miceTime to occlusion (min)
TotalNo occlusionTransient occlusionComplete occlusion
Control WT PBS – 15 ± 0.5 
Control HB PBS – >30 
Experimental, 10 minutes after injury         
 Wild-type HB wt-FXa 450 >30 
 Group 1 HB FXa-V17M 450 3.2 ± 0.3 
 Group 2 HB FXa-I16M 450 2.0 ± 0.1 
 Group 3 HB FXa-I16T 450 3.3 ± 0.3 
Experimental, 15 minutes before injury         
 Group 1 HB FXa-V17M 450 >30 
 Group 2 HB FXa-I16M 450 7.1 
 Group 3 HB FXa-I16T 450 7.6 ± 1.2 
HB FXa-I16T 225 12 ± 0.7 
HB FXa-I16T 113 13 ± 1 
HB FXa-I16T 56 12 
GroupGenotype*SampleDose (µg/kg)No. of miceTime to occlusion (min)
TotalNo occlusionTransient occlusionComplete occlusion
Control WT PBS – 15 ± 0.5 
Control HB PBS – >30 
Experimental, 10 minutes after injury         
 Wild-type HB wt-FXa 450 >30 
 Group 1 HB FXa-V17M 450 3.2 ± 0.3 
 Group 2 HB FXa-I16M 450 2.0 ± 0.1 
 Group 3 HB FXa-I16T 450 3.3 ± 0.3 
Experimental, 15 minutes before injury         
 Group 1 HB FXa-V17M 450 >30 
 Group 2 HB FXa-I16M 450 7.1 
 Group 3 HB FXa-I16T 450 7.6 ± 1.2 
HB FXa-I16T 225 12 ± 0.7 
HB FXa-I16T 113 13 ± 1 
HB FXa-I16T 56 12 

In HB mice, protein was infused 10 minutes after or 15 minutes before 7.5% FeCl3 exposure. Data for mice presenting with no occlusion, transient occlusion, or complete occlusion of the carotid artery following FeCl3 exposure are provided. Occlusion time measurements are presented as mean ± SEM and are derived from both transient and complete events.

*

HB, hemophilia B mice; WT, hemostatically normal mice.

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