Cigarette smoking is a risk factor for development of cardiovascular (CV) disease [1], with increased platelet activation due to cigarette smoke involving a major part of this risk.[2] We have shown that this smoke-induced platelet activation is largely due to the non-nicotine smoke components and their effects can be effectively modulated in the presence of nicotine.[3] However, the effects of nicotine and non-nicotine cigarette smoke components need to be confirmed more physiologically in the presence of endothelial cells (ECs). Prior in-vitro studies have shown that high concentrations of cigarette smoke extract (CSE) increase adhesion molecule expression on ECs.[4] These studies however preclude the involvement of physiological shear stresses and are performed on ECs alone. To overcome these limitations and investigate ECs-platelets together in one system under shear stress, we use a hemodynamic shear device (HSD) that combines features of the cone and plate, and the annular Couette viscometer (to facilitate platelet sampling). We test the following hypotheses — (1) smoke-activated platelets and the nicotine-free extract would confer a synergistic E-selectin expression on ECs, and (2) in contrast to conventional cigarette extracts, nicotine-free smoke extracts would increase platelet activation more significantly, and that this effect may be independent of the presence of ECs.

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