A Single Controlled Exposure to Secondhand Smoke May Not Alter Thrombogenesis or Trigger Platelet Activation.

Autor:	Srikanth S; Division of Cardiovascular Medicine, University of California San Francisco, Fresno, CA., Sy F; Division of Cardiovascular Medicine, University of California San Francisco, Fresno, CA., Kotak K; Division of Cardiovascular Medicine, University of California San Francisco, Fresno, CA., Kiel RG; Division of Cardiovascular Medicine, University of California San Francisco, Fresno, CA., Bajwa M; Division of Cardiovascular Medicine, University of California San Francisco, Fresno, CA., Tandon A; Division of Cardiovascular Medicine, University of California San Francisco, Fresno, CA., Loures-Vale AA; Division of Cardiovascular Medicine, University of California San Francisco, Fresno, CA., Aftab W; Division of Cardiovascular Medicine, University of California San Francisco, Fresno, CA., Tringali S; Division of Cardiovascular Medicine, University of California San Francisco, Fresno, CA., Ambrose JA; Division of Cardiovascular Medicine, University of California San Francisco, Fresno, CA jamambrose@yahoo.com.
Jazyk:	angličtina
Zdroj:	Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco [Nicotine Tob Res] 2016 May; Vol. 18 (5), pp. 580-4. Date of Electronic Publication: 2015 Jun 22.
DOI:	10.1093/ntr/ntv133
Abstrakt:	Introduction: Chronic secondhand smoke (SHS) exposure increases cardiovascular events, particularly acute thrombotic events. There are little human data on acute SHS exposure. The aim of this study was to determine whether a single controlled exposure of humans to SHS increased thrombogenesis. Methods: After 6-8 hours fast, subjects (n = 50) were exposed to constant dose SHS (particulate level of 500 μg/m(3)) for 120 minutes in a temperature-regulated and ventilated, simulated bar environment. Blood was drawn before and immediately after SHS exposure for thromboelastography (TEG) and flow cytometry. Maximum clot strength (MA) was measured using TEG and platelet leukocyte aggregates (LPA) were measured as an index of platelet activation. Anti-CD 14 antibodies were used as leukocyte markers and anti-CD 41 antibodies as platelet markers for cytometry. Data were analyzed using students' t test for paired samples. Results: There was no effect of acute exposure to SHS on platelet activation or thrombogenesis. Also, intra group (smokers [n = 19] and nonsmokers [n = 31]) comparisons of LPA and TEG parameters did not show changes with SHS exposure. Conclusions: While there are abundant data showing enhanced thrombogenesis and platelet activation following repeated exposure to SHS, our study suggests that a single exposure does not appear to significantly alter thrombin kinetics nor result in platelet activation. The effects of SHS on thrombogenesis might be nonlinear. (© The Author 2015. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)
Databáze:	MEDLINE
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