Fig. 1.
Fig. 1. Effect of freeze-fractured platelets and platelet activation on the APTT. In each panel, the vertical axis is the APTT in seconds in the presence of APC (•) and in the absence of APC (○). Error bars indicate standard error of the mean. In (A), the effect of freeze-fracturing is shown. In the absence of APC, the APTT was constant, but in the presence of APC, the APTT was reduced even at a platelet count of 2 × 109/L. In the example shown, the APC sensitivity ratio of PPP and fresh PRP was 3.2. This was reduced in freeze-fractured PRP to a ratio of 1.7 at a platelet count of 400 × 109/L. After ultracentrifugation at 77,000g for 1 hour, the APC resistance phenotype was abolished (▪). In (B, C, and D), the effect of platelet activation with different agonists is shown: (B) TRAP (n = 3); (C) collagen (n = 7); and (D) A23187 (n = 3).

Effect of freeze-fractured platelets and platelet activation on the APTT. In each panel, the vertical axis is the APTT in seconds in the presence of APC (•) and in the absence of APC (○). Error bars indicate standard error of the mean. In (A), the effect of freeze-fracturing is shown. In the absence of APC, the APTT was constant, but in the presence of APC, the APTT was reduced even at a platelet count of 2 × 109/L. In the example shown, the APC sensitivity ratio of PPP and fresh PRP was 3.2. This was reduced in freeze-fractured PRP to a ratio of 1.7 at a platelet count of 400 × 109/L. After ultracentrifugation at 77,000g for 1 hour, the APC resistance phenotype was abolished (▪). In (B, C, and D), the effect of platelet activation with different agonists is shown: (B) TRAP (n = 3); (C) collagen (n = 7); and (D) A23187 (n = 3).

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