Differences between mainstream and sidestream cigarette smoke extracts and nicotine in the activation of platelets under static and flow conditions.

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 micromol/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.