Journal
JOURNAL OF SURGICAL RESEARCH
Volume 116, Issue 2, Pages 227-233Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S0022-4804(03)00343-3
Keywords
smoking; CD62; endothelium; von Willebrand Factor; nitric oxide; aggregation
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Background. Cigarette smoking results in abnormalities of platelets and endothelium with platelet dysfunction implicated in vascular complications. Healthy endothelium plays a pivotal role in regulating hemostasis via the inhibition of platelet activation and aggregation. Thus, we examined if platelet dysfunction correlated with serum vWF levels-a circulating marker of endothelial dysfunction. Materials and methods. We tested this hypothesis in young male smokers. The parameters of platelet function tested included: CD62/CD63; Glycoprotein (GP) IIb/IIIa; Platelet function analzyer (PFA) studies, platelet aggregometry, flow assessment of platelet microparticles, platelet-leukocyte interactions and receptor numbers. Endothelial dysfunction was assessed with serum von Willebrand Factor (vWF). Results. There was a significant increase in platelet CD62 receptor expression and aggregation with an associated delay in time to aggregation using PFA. Endothelial dysfunction was represented by higher serum levels of von Willebrand Factor. All other platelet parameters tested were within the standardized reference range. Conclusions. These initial data suggests that antiplatelet therapy may have a role in reduction of platelet activation and aggregation in young smokers and possibly alter vascular endothelial abnormalities. (C) 2004 Elsevier Inc. All rights reserved.
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