Brief Reviews |
From the VA New York Harbor Healthcare System and Weill Medical College of Cornell University (A.J.M., M.J.B., J.H.F.D., N.I.), New York, NY; Columbia University College of Physicians and Surgeons (D.J.P.), New York, NY; and Immunex Corp (R.B.G., C.R.M.), Seattle, Wash.
Correspondence to Aaron J. Marcus, MD, Chief, Hematology/Medical Oncology, VA New York Harbor Healthcare System, 423 East 23rd St, Room 13028W, New York, NY 10010. E-mail ajmarcus{at}med.cornell.edu
AbstractDuring their 7- to 9-day lifespan in the circulation, platelets perform an ill-defined baseline function that maintains the integrity of the vasculature. In thrombocytopenic states, there is an increase in vascular permeability and fragility, which is presumably due to absence of this platelet function. In sharp contrast, biochemical or physical injury in the coronary, carotid, or peripheral arteries induces platelet activation and platelet recruitment, which can progress to thrombotic vascular occlusion. Because there is 1 death every 33 seconds from vascular occlusion in the United States, this problem has critical public health implications. In this review, we describe the characterization of a novel potential antithrombotic agent with a unique mode of actionbiochemical "deletion" of ADP from an activated platelet releasate, which thereby inhibits platelet recruitment and further activation.
Key Words: endothelial cells thrombosis platelets CD39/ecto-ADPase
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