Figure 6.
Activation of thrombin-activatable fibrinolysis inhibitor (TAFI) under flow conditions. (A) Thrombogenicity of different platelet concentrations of whole blood (WB), supplemented with 5 nM tissue-type plasminogen activator was examined using Total Thrombus formation Analysis System (T-TAS). Representative pressure changes are indicated as color lines: pink, platelet-rich WB; blue, normal WB; green, 50% normal and 50% platelet-poor (platelet-half) WB; orange and red, platelet-poor WB. (B) Thrombogenicity-related parameters (T10 [red bars]: time to 10-kPa increase, OT [blue bars]: occlusion time, AUC30 [green line]: area under the curve for 30 minutes) in platelet-poor (80-kPa increase achieved in just 1 sample [74 × 109/L platelets]; the other 2 samples did not achieve an 80-kPa increase within 30 minutes), platelet-half (n = 4, 162 ± 16 [average ± SD] × 109/L platelets), normal (n = 4, 293 ± 7.8 [average ± SD] × 109/L platelets), and platelet-rich (n = 7, 376 ± 65 [average ± SD] × 109/L platelets) WB are displayed. Statistical analysis was performed using Williams multiple comparison (*P < .01 against platelet-half WB). (C-E) Thrombogenicity in platelet-half WB, with or without 5 nM tissue-type plasminogen activator (tPA) or 10 μM activated TAFI inhibitor (TAFIaI), was examined at a shear rate of 240 seconds−1. Sample numbers are as follows (tPA/TAFIaI): −/−, +/−, −/+, and +/+, n = 6, n = 6, n = 3, and n = 6, respectively. (C) T10 is shown as the average ± SD. No significant change was determined by Student t test. OT (D) and AUC30 (E) are shown as the median and interquartile range and were analyzed using the Mann-Whitney U test (#P < .01 vs tPA−/TAFIaI−, +P < .05). Two samples treated with both tPA and TAFIaI, which did not achieve an 80-kPa increase within 1800 seconds, are represented as closed 2 circles in panel D. Four individuals donated blood to these experiments.

Activation of thrombin-activatable fibrinolysis inhibitor (TAFI) under flow conditions. (A) Thrombogenicity of different platelet concentrations of whole blood (WB), supplemented with 5 nM tissue-type plasminogen activator was examined using Total Thrombus formation Analysis System (T-TAS). Representative pressure changes are indicated as color lines: pink, platelet-rich WB; blue, normal WB; green, 50% normal and 50% platelet-poor (platelet-half) WB; orange and red, platelet-poor WB. (B) Thrombogenicity-related parameters (T10 [red bars]: time to 10-kPa increase, OT [blue bars]: occlusion time, AUC30 [green line]: area under the curve for 30 minutes) in platelet-poor (80-kPa increase achieved in just 1 sample [74 × 109/L platelets]; the other 2 samples did not achieve an 80-kPa increase within 30 minutes), platelet-half (n = 4, 162 ± 16 [average ± SD] × 109/L platelets), normal (n = 4, 293 ± 7.8 [average ± SD] × 109/L platelets), and platelet-rich (n = 7, 376 ± 65 [average ± SD] × 109/L platelets) WB are displayed. Statistical analysis was performed using Williams multiple comparison (*P < .01 against platelet-half WB). (C-E) Thrombogenicity in platelet-half WB, with or without 5 nM tissue-type plasminogen activator (tPA) or 10 μM activated TAFI inhibitor (TAFIaI), was examined at a shear rate of 240 seconds−1. Sample numbers are as follows (tPA/TAFIaI): −/−, +/−, −/+, and +/+, n = 6, n = 6, n = 3, and n = 6, respectively. (C) T10 is shown as the average ± SD. No significant change was determined by Student t test. OT (D) and AUC30 (E) are shown as the median and interquartile range and were analyzed using the Mann-Whitney U test (#P < .01 vs tPA−/TAFIaI−, +P < .05). Two samples treated with both tPA and TAFIaI, which did not achieve an 80-kPa increase within 1800 seconds, are represented as closed 2 circles in panel D. Four individuals donated blood to these experiments.

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