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A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry

Published on: June 5, 2019

Downstream platelet adhesion and activation under highly elevated upstream shear forces.

Shekh M Rahman¹, Vladimir Hlady²

¹Department of Chemical Engineering, University of Utah, Salt Lake City, USA.

Acta Biomaterialia

|April 21, 2019

Summary

This summary is machine-generated.

Transient exposure to high shear forces, like those near vascular graft stenosis, primes platelets for increased downstream adhesion and activation. This can lead to thrombus formation, highlighting risks with blood-contacting devices.

Keywords:

Anastomotic stenosis Flow cytometry Microfluidics Platelet adhesion and activation Platelet lysis

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Last Updated: Jan 26, 2026

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Published on: June 5, 2019

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Area of Science:

Biomedical Engineering
Hemodynamics
Thrombosis Research

Background:

Anastomotic stenosis in vascular implants causes elevated shear forces, leading to platelet aggregation.
The downstream effects of transiently elevated shear forces on platelet pre-activation are not well understood.
Understanding these effects is crucial for assessing thrombotic risks of blood-contacting devices.

Purpose of the Study:

To investigate how transient exposure to elevated shear forces affects platelet adhesion and activation.
To explore the role of altered hemodynamics in thrombus formation downstream of stenosis.
To inform the design of blood-contacting biomaterials to minimize thrombotic risk.

Main Methods:

Developed a microfluidic flow system simulating vascular stenosis.
Exposed whole blood to varying wall shear strain rates (1620–11560 s⁻¹).
Assessed downstream platelet adhesion and activation marker expression.

Main Results:

Transient elevated shear forces increased downstream platelet adhesion to fibrinogen, collagen, and von Willebrand factor.
Significant increases in platelet activation markers (P-selectin, GPIIb/IIIa, etc.) were observed at higher shear rates (2975–11560 s⁻¹).
Platelet lysis occurred at the highest shear rate (11560 s⁻¹).

Conclusions:

Elevated shear forces near anastomotic stenosis pre-activate platelets, enhancing downstream adhesion and activation.
These findings provide insights into thrombus formation mechanisms post-stenosis.
Optimizing biomaterial design to mitigate shear-induced platelet activation is critical for vascular implants.