Duration of exposure to high fluid shear stress is critical in shear-induced platelet activation-aggregation

Zhang Jian-ning; Angela L. Bergeron; Qinghua Yu; Carol Sun; Latresha McBride; Paul F. Bray; Jing-fei Dong

doi:10.1160/TH03-03-0145

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 2003; 90(04): 672-678
DOI: 10.1160/TH03-03-0145

Platelets and Blood Cells

Schattauer GmbH

Duration of exposure to high fluid shear stress is critical in shear-induced platelet activation-aggregation

Authors

Zhang Jian-ning

¹Section of Thrombosis Research, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA

^‡Current address: Department of Neurosurgery, Tianjin General Hospital, Tianjin Medical University, Tianjin, China
Angela L. Bergeron

¹Section of Thrombosis Research, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA
Qinghua Yu

¹Section of Thrombosis Research, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA
Carol Sun

¹Section of Thrombosis Research, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA
Latresha McBride

¹Section of Thrombosis Research, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA
Paul F. Bray

¹Section of Thrombosis Research, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA
Jing-fei Dong

¹Section of Thrombosis Research, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA

Abstract

Summary

Platelet functions are increasingly measured under flow conditions to account for blood hydrodynamic effects. Typically, these studies involve exposing platelets to high shear stress for periods significantly longer than would occur in vivo. In the current study, we demonstrate that the platelet response to high shear depends on the duration of shear exposure. In response to a 100 dyn/cm² shear stress for periods less than 10-20 sec, platelets in PRP or washed platelets were aggregated, but minimally activated as demonstrated by P-selectin expression and binding of the activation-dependent αIIbβ₃ antibody PAC-1 to sheared platelets. Furthermore, platelet aggregation under such short pulses of high shear was subjected to rapid disaggregation. The disaggregated platelets could be re-aggregated by ADP in a pattern similar to unsheared platelets. In comparison, platelets that are exposed to high shear for longer than 20 sec are activated and aggregated irreversibly. In contrast, platelet activation and aggregation were significantly greater in whole blood with significantly less disaggregation. The enhancement is likely via increased collision frequency of platelet-platelet interaction and duration of platelet-platelet association due to high cell density. It may also be attributed to the ADP release from other cells such as red blood cells because increased platelet aggregation in whole blood was partially inhibited by ADP blockage. These studies demonstrate that platelets have a higher threshold for shear stress than previously believed. In a pathologically relevant timeframe, high shear alone is likely to be insufficient in inducing platelet activation and aggregation, but acts synergistically with other stimuli.

Keywords

Shear stress - stenosis - platelet activation - aggregation

Full Text

References

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