An ex-vivo model of shear-rate-based activation of blood coagulation

Marco Ranucci1, Matteo Ranucci, Ekaterina Baryshnikova

  • 1Department of Cardiothoracic - Vascular Anesthesia and Intensive Care, IRCCS Policlinico San Donato, Milan, Italy.

: The study presents a model of shear-stress-based platelet activation. Twenty-eight patients (22 free from anticoagulants and major antiplatelet agents, and six under the effects of P2Y12 platelet inhibitors) participated. The main purpose was to verify the hypothesis that a model of shear-dependent blood activation does not require artificial activators to trigger clot formation. Whole blood collected from the patients received platelet function tests [ADPtest and thrombin receptor-activating peptide (TRAP)test] and was tested with a cone-on-plate viscosimeter at a shear rate of 100 s. Changes in blood viscosity were characterized by a time-to-gel point (TGP), a maximum clot viscosity and a steady clot viscosity (SCV). In patients free from major antiplatelet effects, the TGP was 180 s (interquartile range 148-290 s), while in patients under double antiplatelet therapy the TGP was significantly (P = 0.039) longer (345 s, interquartile range 250-452 s). The SCV was 16 centipoise (cP) (interquartile range 11-47 cP) in the patients free from major antiplatelet agents, significantly (P = 0.012) higher than in patients under double antiplatelet therapy (10 cP, interquartile range 6-11 cP). There was a significant (P = 0.011) association between platelet function at the TRAPtest and the maximum clot viscosity, and between TRAPtest and the SCV (P = 0.021). A shear rate of 100 s triggers clot formation through a primary role of platelet activation in this model of blood activation.

Related Concept Videos

Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
13.4K
Coagulation01:09

Coagulation

The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
10.8K
Coagulation01:06

Coagulation

Colloidal solids are solid particles suspended in solution. They are usually negatively charged, attracting a compact primary layer of positively charged ions, which attract more counterions to form an electrical double layer. Electrostatic repulsion between the charged double layers prevents the particles from colliding, stabilizing the colloids. These solids are often undesirable because they can contain toxins that are difficult to remove. Coagulation is a technique that helps aggregate and...
1.5K