The structural integrity of platelet receptors is essential for platelets to play the normal hemostatic function. The high non-physiologic shear stress (NPSS) commonly exists in blood-contacting medical devices and has been shown to cause platelet receptor shedding. The loss of platelet receptors may impair the normal hemostatic function of platelets. The aim of this study was to quantify NPSS-induced shedding of three key receptors on the platelet surface. Human blood was subjected to the matrix of well-defined shear stresses and exposure times, generated by using a custom-designed blood-shearing device. The expression of three key platelet receptors, glycoprotein (GP) Ibα, GPVI, and GPIIb/IIIa, in sheared blood was quantified using flow cytometry. The quantitative relationship between the loss of each of the three receptors on the platelet surface and shear condition (shear stress level and exposure time) was explored. It was found that these relationships followed well the power law functional form. The coefficients of the power law models for the shear-induced shedding of these platelet receptors were derived with coefficients of determination (R 2) of 0.77, 0.73, and 0.78, respectively. The power law models with these coefficients may be potentially used to predict the shear-induced platelet receptor shedding of human blood.
From the *Artificial Organs Laboratory, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland
†Fischell Department of Bioengineering, University of Maryland, College Park, Maryland
‡Department of Cardiovascular and Thoracic Surgery, University of Louisville School of Medicine, Louisville, Kentucky.
Submitted for consideration June 2017; accepted for publication in revised form September 2017.
Disclosure: The authors have no conflicts of interest to report.
Supported partially by the National Institutes of Health (Grant number: R01HL 124170).
Correspondence: Zhongjun J. Wu, PhD, Department of Surgery, University of Maryland School of Medicine, 10 South Pine Street, MSTF 434A, Baltimore, MD 21201. Email: email@example.com.