Table 1.
Time to carotid artery occlusion following FeCl3-induced injury.
| Genotype | Sample | Dose | Total # of mice |
No Occlusion |
Transient Occlusion |
Complete Occlusion |
Time to Occlusion |
|---|---|---|---|---|---|---|---|
| µg/kg | # of mice | # of mice | # of mice | # of mice | min | ||
| Controls | |||||||
| WT (Balb/c) | PBS | -- | 7 | 0 | 0 | 7 | 10.1 ± 1.0 |
| HB (Balb/c) | PBS | -- | 7 | 7 | 0 | 0 | -- |
| WT (C57BL/6) | PBS | -- | 4 | 0 | 0 | 4 | 11.9 ± 1.0 |
| HB (C57BL/6) | PBS | -- | 4 | 4 | 0 | 0 | -- |
| HB (Balb/c) | hFIX | 500 | 5 | 0 | 0 | 5 | 14.6 ± 1.1 |
| Experimental—Human Proteins | |||||||
| HB (Balb/c) | hFXaI16L | 90 | 5 | 0 | 3 | 2 | 3.2 ± 0.6 |
| HB (Balb/c) | hFXaI16L | 180 | 3 | 0 | 0 | 3 | 2.4 ± 0.6 |
| HB (Balb/c) | hFXaI16L | 450 | 10 | 0 | 0 | 10 | 2.2 ± 0.2 |
| HB (C57BL/6) | hFXaI16L | 450 | 4 | 0 | 0 | 4 | 1.2 ± 0.1 |
| HB (Balb/c) | hFVIIa | 1,000 | 4 | 2 | 1 | 1 | 3.4 ± 0.1 |
| HB (Balb/c) | hFVIIa | 3,000 | 3 | 0 | 2 | 1 | 3.3 ± 0.3 |
| HB (Balb/c) | hFVIIa | 5,000 | 4 | 0 | 0 | 4 | 2.4 ± 0.2 |
| Experimental—Murine Proteins | |||||||
| HB (Balb/c) | mFXaI16L | 50 | 3 | 0 | 2 | 1 | 2.6 ± 0.4 |
| HB (Balb/c) | mFXaI16L | 100 | 5 | 0 | 1 | 4 | 2.3 ± 0.4 |
| HB (Balb/c) | mFVIIa | 500 | 3 | 3 | 0 | 0 | -- |
| HB (Balb/c) | mFVIIa | 3,000 | 7 | 5 | 0 | 2 | 2.4 ± 0.1 |
| HB (Balb/c) | mFVIIa | 5,000 | 4 | 0 | 0 | 4 | 2.5 ± 0.2 |
WT, hemostatically normal mice; HB, hemophilia B mice; PBS, phosphate buffer saline, FIX, factor IX.
The total number of mice per experiment is indicated. In HB mice, protein was infused 10 min after FeCl3 exposure. Mice presenting with no occlusion, transient occlusion or complete occlusion of the carotid artery following FeCl3 exposure is tabulated. Occlusion time measurements are presented as mean ± SEM and are derived from both transient and complete events. Representative Doppler blood flow versus time tracings can be found in Supplemental Fig. 4.