Figure 4.
Figure 4. Efficacy of line h38 platelet hemostatic efficacy in mice. (A-D) FeCl3 carotid artery injury studies were as described.17 Area under the curve (AUC) of subsequent blood flow was measured. In all studies, P values were determined by 1-way analysis of variance. (A) WT, FVIIInull, and line h38 mice were studied, as were FVIIInull mice infused with either WT or line h38 platelets to achieve ∼20% of the circulating platelets in the recipient. Animals infused with line h38 platelets were studied up to 72 hours later. Mean ± 1 standard error of the mean (SEM) are shown, with 5 animals per arm. (B) Same as in panel A, with studied FVIIInull mice infused with the indicated amounts of line h38 platelets and rFVIIa. Mean ± 1 SEM are shown, with 5 animals per arm. (C) Line h38 mice were infused with varying concentrations of the inhibitor mixture (in milligrams per kilogram of mouse) before the FeCl3 injury. Mean ± 1 SEM are shown, with 6 animals per arm. (D) FVIIInull and line h38 mice were studied in the FeCl3 carotid artery injury model, as in panel A. FVIIInull mice were also infused with ∼15% line h38 or WT platelets and with varying concentrations of the inhibitor mixture (in milligrams per kilogram of mouse) ± 1 mg/kg of rFVIIa before the FeCl3 injury. Mean ± 1 SEM are shown, with 5 animals per arm. (E) Tail-clip exsanguination studies, as in Figure 3. Mice received either h38 platelets or human FVIII infusions at 0.125 U/mL of blood. Tail-clip exsanguination studies were delayed for 0 to 24 hours after h38 platelet infusion as indicated. Number of mice studied is indicated in each bar.

Efficacy of line h38 platelet hemostatic efficacy in mice. (A-D) FeCl3 carotid artery injury studies were as described.17  Area under the curve (AUC) of subsequent blood flow was measured. In all studies, P values were determined by 1-way analysis of variance. (A) WT, FVIIInull, and line h38 mice were studied, as were FVIIInull mice infused with either WT or line h38 platelets to achieve ∼20% of the circulating platelets in the recipient. Animals infused with line h38 platelets were studied up to 72 hours later. Mean ± 1 standard error of the mean (SEM) are shown, with 5 animals per arm. (B) Same as in panel A, with studied FVIIInull mice infused with the indicated amounts of line h38 platelets and rFVIIa. Mean ± 1 SEM are shown, with 5 animals per arm. (C) Line h38 mice were infused with varying concentrations of the inhibitor mixture (in milligrams per kilogram of mouse) before the FeCl3 injury. Mean ± 1 SEM are shown, with 6 animals per arm. (D) FVIIInull and line h38 mice were studied in the FeCl3 carotid artery injury model, as in panel A. FVIIInull mice were also infused with ∼15% line h38 or WT platelets and with varying concentrations of the inhibitor mixture (in milligrams per kilogram of mouse) ± 1 mg/kg of rFVIIa before the FeCl3 injury. Mean ± 1 SEM are shown, with 5 animals per arm. (E) Tail-clip exsanguination studies, as in Figure 3. Mice received either h38 platelets or human FVIII infusions at 0.125 U/mL of blood. Tail-clip exsanguination studies were delayed for 0 to 24 hours after h38 platelet infusion as indicated. Number of mice studied is indicated in each bar.

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