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Circulation. 2004;109:78-83
Published online before print December 22, 2003, doi: 10.1161/01.CIR.0000108395.12766.25
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(Circulation. 2004;109:78-83.)
© 2004 American Heart Association, Inc.


Clinical Investigation and Reports

Differences Between Mainstream and Sidestream Cigarette Smoke Extracts and Nicotine in the Activation of Platelets Under Static and Flow Conditions

David Rubenstein; Jolyon Jesty, PhD; Danny Bluestein, PhD

From the Department of Biomedical Engineering (D.R., D.B.) and the Division of Hematology, School of Medicine (J.J.), Stony Brook University, Stony Brook, New York.

Correspondence to Danny Bluestein, PhD, Department of Biomedical Engineering, Health Sciences Center, Stony Brook University, Stony Brook, NY 11794-8181. E-mail danny.bluestein{at}sunysb.edu

Received March 24, 2003; de novo received July 17, 2003; revision received September 19, 2003; accepted September 22, 2003.

Background— Cigarette smoke is a primary risk factor for cardiovascular diseases. Enhanced function of the hemostatic system, in which platelets play a major role, is a significant underlying mechanism in cardiovascular disease and its progression. Epidemiological studies, complemented by physiological and biochemical data, show that cigarette smoke adversely affects platelet function, both in smokers and in nonsmokers exposed to sidestream smoke.

Methods and Results— The thrombogenic potential of platelets subjected to mainstream smoke extracts, sidestream extracts, and nicotine was measured in vitro under static and dynamic flow conditions. Platelet activation state was measured with a modified prothrombinase-based method. Mainstream and sidestream smoke extracts caused increased platelet activation. Although low-tar mainstream extracts activated platelets less than high-tar extracts, the sidestream extracts were almost equally potent. Modification of the filters of low-tar cigarettes, by blocking the air-bypass holes, raised activation rates by mainstream extracts to the level of high-tar extracts. Nicotine (50 nmol/L and 5 µmol/L) inhibited platelet activation under both flow and static conditions.

Conclusions— Cigarette smoke extracts directly cause platelet activation but also markedly increase the susceptibility of platelets to activation by shear stress. In contrast, nicotine, although also a constituent of cigarette smoke, significantly reduces platelet susceptibility to shear stress.


Key Words: platelets • smoking • thrombosis • cardiovascular diseases




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