Abstract
Cigarette smoking is a major risk factor for acute coronary thrombosis. In fact, both active/first-hand smoke and passive/second-hand smoke exposure are known to increase the risk of coronary thrombosis. Although recently a new risk has been identified and termed third-hand smoke (THS), which is the residual tobacco smoke contaminant that remains after a cigarette is extinguished, it remains to be determined whether it can also enhance the risk of thrombogenesis, much like first-hand smoke and second-hand smoke. Therefore, the present studies investigated the impact of THS exposure in the context of platelet biology and related disease states. It was found that THS-exposed mice exhibited an enhanced platelet aggregation and secretion responses as well as enhanced integrin GPIIb-IIIa activation. Furthermore, it was found that THS exposure shortens the tail bleeding time and the occlusion time in a model of thrombosis. Thus, our data demonstrate for the first time (at least in mice) that THS exposure increases the risk of thrombosis-based disease states, which is attributed, at least in part, to their hyperactive platelets.
Original language | English (US) |
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Pages (from-to) | 177-182 |
Number of pages | 6 |
Journal | Journal of Cardiovascular Pharmacology |
Volume | 66 |
Issue number | 2 |
DOIs | |
State | Published - Aug 21 2015 |
Externally published | Yes |
Keywords
- hemostasis
- Platelet
- third-hand smoke
- thrombogenesis
- tobacco
ASJC Scopus subject areas
- Pharmacology
- Cardiology and Cardiovascular Medicine