Paper Number
BB4 

Session
Biomaterials and Biological Systems

Title
Microrheological study of plasma coagulation triggered by intrinsic pathway

Presentation Date and Time
October 11, 2017 (Wednesday) 11:05

Track / Room
Track 1 / Crystal A

Authors (Click on name to view author profile)

1. Mao, Yating (Oregon State University, CBEE)
2. Tan, Mingyang (Oregon State University, CBEE)
3. McCarty, Owen J. (Oregon Health & Science University, Biomedical Engineering)
4. Walker, Travis W. (Oregon State University, CBEE)

Author and Affiliation Lines (in printed abstract book)
Yating Mao¹, Mingyang Tan¹, Owen J. McCarty², and Travis W. Walker^1
1CBEE, Oregon State University, Corvallis, OR 97331; ²Biomedical Engineering, Oregon Health & Science University, Portland, OR 97239

Speaker / Presenter 
Walker, Travis W.

Text of Abstract
Both the extrinsic pathway, caused by tissue injury, and the intrinsic pathway, initiated by the exposure to a negatively charged surface, can initiate fibrin clot formation. At the early stages of the intrinsic pathway, FXII is converted to FXIIa, which then activates FXI. The structure of the fibrin is crucial for the kinetics and stability of thrombus formation, controlling the strength of the clot and its susceptibility to lysis. To measure the role of FXI in the coagulation kinetics and the fibrin clot structure, standard microrheology is performed on platelet-poor plasma to extract the transient rheological properties of the fibrin clots that are formed with and without the inhibition of FXI. The rheological change of fibrin gel is indicated by the decreasing diffusivity of probe particles that are dispersed in the plasma. At the late stage of the coagulation, a sub-diffusive region becomes notable, and a static mean squared displacement indicates the completion of the coagulation.