Thromb Haemost 2002; 88(05): 817-821
DOI: 10.1055/s-0037-1613308
Review Article
Schattauer GmbH

Platelet Aggregation and Activation under Complex Patterns of Shear Stress

Jian-ning Zhang
1  The Division of Thrombosis Research, Department of Medicine, Houston, TX
,
Angela L. Bergeron
1  The Division of Thrombosis Research, Department of Medicine, Houston, TX
,
Qinghua Yu
1  The Division of Thrombosis Research, Department of Medicine, Houston, TX
,
Carol Sun
1  The Division of Thrombosis Research, Department of Medicine, Houston, TX
,
Larry V. McIntire
3  Cox Laboratory for Bioengineering, Rice University, Houston, TX, USA
,
José A. López
1  The Division of Thrombosis Research, Department of Medicine, Houston, TX
2  Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX
,
Jing-fei Dong
1  The Division of Thrombosis Research, Department of Medicine, Houston, TX
› Author Affiliations
This work was supported by NIH grants HL64796, 1-P50-HL65967, HL18673; and a Grant-in-Aid from the American Heart Association-Texas Affiliate
Further Information

Publication History

Received 14 January 2002

Accepted after resubmission 02 July 2002

Publication Date:
08 December 2017 (online)

Summary

Arterial stenosis results in a complex pattern of blood flow containing an extremely fast flow in the throat of stenosis and a post-stenosis low flow. The fast flow generates high shear stress that has been demonstrated in vitro to activate and aggregate platelets. One potential problem of these in vitro studies is that platelets are invariably exposed to a high shear stress for a period that is significantly longer than they would have experienced in vivo. More importantly, the role of the poststenosis low flow in platelet activation and aggregation has not been determined. By exposing platelets to a shear profile that contains both high and low shear segments, we found that platelets aggregate when they are exposed to a high shear stress of 100 dyn/cm2 for as short as 2.5 s, a period that is significantly shorter than those previously reported (30–120 s). Platelet aggregation under this condition requires a low shear exposure immediately after a high shear pulse, suggesting that post-stenosis low flow enhances platelet aggregation. Furthermore, platelet aggregation under this condition is not activation-dependent because the CD62P expression of sheared platelets is significantly less than that of platelets treated with ADP. Based on these findings, we propose that shear-induced platelet aggregation may be a process of mechanical crosslinking of platelets, requiring minimal platelet activation. This process may function as a protective mechanism to prevent in vivo irreversible platelet activation and aggregation under temporary high shear.