Figure 3.
Lack of PS in platelets affects global hemostasis assessment ex vivo and in vivo. (A-B) Whole blood activation of coagulation and clot polymerization determined by ROTEM analysis rotational (thromboelastography). (A) Extrinsic‐activated rotational thromboelastometry (EXTEM) assay, (B) extrinsically activated thromboelastometric test with cytochalasin D (FIBTEM). CT, coagulation time; CFT, clot formation time; α, α-angle; CFR, clot formation rate, MCF, maximum clot firmness; MCE, maximum clot elasticity. (C-D) Total thrombus-formation analysis on whole blood on collagen and TF-coated chip (AR-chip) at low (240 s−1, C) and high (600 s−1, D) shear rate. (E-F) Bleeding time (E) and blood loss (F) were measured after 2-mm tail transection in Pros1lox/loxPf4-Cre− (n = 7), Pros1lox/loxPf4-Cre+ (n = 7), and Pros1lox/− (n = 5) mice. All data are expressed as mean ± SEM. ns, not significant; *P < .05; **P ≤ .01; ***P ≤ .001.

Lack of PS in platelets affects global hemostasis assessment ex vivo and in vivo. (A-B) Whole blood activation of coagulation and clot polymerization determined by ROTEM analysis rotational (thromboelastography). (A) Extrinsic‐activated rotational thromboelastometry (EXTEM) assay, (B) extrinsically activated thromboelastometric test with cytochalasin D (FIBTEM). CT, coagulation time; CFT, clot formation time; α, α-angle; CFR, clot formation rate, MCF, maximum clot firmness; MCE, maximum clot elasticity. (C-D) Total thrombus-formation analysis on whole blood on collagen and TF-coated chip (AR-chip) at low (240 s−1, C) and high (600 s−1, D) shear rate. (E-F) Bleeding time (E) and blood loss (F) were measured after 2-mm tail transection in Pros1lox/loxPf4-Cre− (n = 7), Pros1lox/loxPf4-Cre+ (n = 7), and Pros1lox/− (n = 5) mice. All data are expressed as mean ± SEM. ns, not significant; *P < .05; **P ≤ .01; ***P ≤ .001.

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