Figure 4
Figure 4. Human platelets do not shorten clotting times by FXII-activating mechanisms. Whole blood coagulation times were measured with the ReoRox instrument, using (A) normal whole blood and (B) FXII-deficient whole blood. A low concentration of TF was added to all samples to minimize the influence of material-induced FXII activation. Samples were either native or activated with the FXII activator celite (5 mg/mL) or platelet activator A23187 (5 μM). CTI (100 μg/mL) or annexin V (1 μg/mL) was used to inhibit the procoagulant activity of FXIIa and negatively charged phospholipids, respectively. Whole blood experiments in normal blood (n = 6-9) and from 2 FXII-deficient individuals are presented as mean ± SD. Statistical testing was performed with ANOVA and Tukey’s post hoc test for normal donors. †Statistical testing of FXII-deficient donors were performed with a paired-samples t test on each donor individually, using 8 repeated measurements per donor.

Human platelets do not shorten clotting times by FXII-activating mechanisms. Whole blood coagulation times were measured with the ReoRox instrument, using (A) normal whole blood and (B) FXII-deficient whole blood. A low concentration of TF was added to all samples to minimize the influence of material-induced FXII activation. Samples were either native or activated with the FXII activator celite (5 mg/mL) or platelet activator A23187 (5 μM). CTI (100 μg/mL) or annexin V (1 μg/mL) was used to inhibit the procoagulant activity of FXIIa and negatively charged phospholipids, respectively. Whole blood experiments in normal blood (n = 6-9) and from 2 FXII-deficient individuals are presented as mean ± SD. Statistical testing was performed with ANOVA and Tukey’s post hoc test for normal donors. Statistical testing of FXII-deficient donors were performed with a paired-samples t test on each donor individually, using 8 repeated measurements per donor.

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