Format

Send to

Choose Destination
Blood Rev. 2011 Jul;25(4):155-67. doi: 10.1016/j.blre.2011.03.002. Epub 2011 Apr 14.

Platelets at work in primary hemostasis.

Author information

1
Laboratory for Thrombosis Research, IRF Life Sciences, KU Leuven Campus Kortrijk, Belgium. Katleen.broos@kuleuven-kortrijk.be

Abstract

When platelet numbers are low or when their function is disabled, the risk of bleeding is high, which on the one hand indicates that in normal life vascular damage is a rather common event and that hence the role of platelets in maintaining a normal hemostasis is a continuously ongoing physiological process. Upon vascular injury, platelets instantly adhere to the exposed extracellular matrix resulting in platelet activation and aggregation to form a hemostatic plug. This self-amplifying mechanism nevertheless requires a tight control to prevent uncontrolled platelet aggregate formation that eventually would occlude the vessel. Therefore endothelial cells produce inhibitory compounds such as prostacyclin and nitric oxide that limit the growth of the platelet thrombus to the damaged area. With this review, we intend to give an integrated survey of the platelet response to vascular injury in normal hemostasis.

PMID:
21496978
DOI:
10.1016/j.blre.2011.03.002
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center