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Updated: Sep 17, 2026
A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
Published on: February 14, 2017
Study of centrifugal blood pump non-physiological shear stress induced platelet hemostatic dysfunction
Yuan Li1, Xiaoning Zhang1, Hongyu Wang1
1Key Laboratory of Biomechanics and Mechanobiology (Beihang University), Ministry of Education, Key Laboratory of Innovation and Transformation of Advanced Medical Devices, Ministry of Industry and Information Technology, National Medical Innovation Platform for Industry-Education Integration in Advanced Medical Devices (Interdiscipline of Medicine and Engineering), School of Biological Science and Medical Engineering, Beihang University, Beijing, 100191, China.
Objective:
To clarify how centrifugal blood pump-induced non-physiological shear stress affects platelet adhesion and aggregation, explaining the coexistence of thrombosis and bleeding during centrifugal pump support.
Methods:
Blood samples collected before and after centrifugal pump operation were used. Platelet adhesion, aggregation, and binding forces were evaluated using collagen and fibrinogen coated microfluidic chips and micropost arrays. Platelet receptor expression, vWF function, and pro-aggregatory factors were further investigated.
Results:
After centrifugal pump operation, platelet adhesion to collagen decreased, especially under higher perfusion shear rates. The platelet and collagen binding force decreased from 33.04 nN to 8.73 nN, indicating impaired adhesive stability. This was associated with reduced platelet GPVI and GPIbα receptor expression, decreased vWF activity, and weakened platelet-vWF binding, suggesting inhibition of both GPVI mediated and vWF/GPIbα mediated adhesion. In contrast, platelet binding to fibrinogen increased, especially under higher perfusion shear rates. The platelet and fibrinogen binding force increased from 12.85 nN to 42.29 nN, indicating enhanced aggregation stability. This was accompanied by increased platelet GPIIb/IIIa receptor activation and elevated pro-aggregatory factors. However, prolonged centrifugal pump operation reduced platelet responsiveness to secondary stimulation and decreased GPIIb/GPIIIa subunit availability, suggesting that sustained shear exposure limits further platelet activation and aggregation.
Conclusion:
Centrifugal blood pump induced non-physiological shear stress impairs collagen mediated initial adhesion while enhancing fibrinogen mediated aggregation. Sustained shear exposure weakens platelet secondary responsiveness and limits further enhancement of aggregation hemostasis. These findings reveal a potential mechanism for the coexistence of thrombosis and bleeding and provide a microfluidic method for hemocompatibility assessment.
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