Passive smoking increases platelet thromboxane |
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Authors: | Harald Kritz Peter Schmid Georgios Karanikas Christian Pirich Yannis Stamatopoulos Bernhard A. Peskar Prof. Helmut Sinzinger M.D. |
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Affiliation: | (1) Wilhelm Auerswald Atherosclerosis Research Group (ASF), Vienna, Nadlergasse 1, A-1090 Vienna, Austria;(2) Rehabilitation Center Engelsbad-Melanie, Baden, Lower Austria, Austria;(3) Department of Nuclear Medicine, University of Vienna, Vienna, Austria;(4) Cardiovascular Rehabilitation Center Bad Schallerbach, Upper Austria, Austria;(5) Department of Pharmacology and Toxicology, Ruhr-University, Bochum, Germany |
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Abstract: | Although active smoking is known to enhance platelet thromboxane production, no data on passive smoking are available yet. In an 18 m3 room, the influence of single and repeated exposure to passive smoke for 60 minutes was assessed in nonsmokers and smokers. Smokers and nonsmokers were matched for sex and age. All the evaluated parameters (plasma TXB2, serum TXB2, malondialdehyde, 11-dehydro-TXB2, conversion of exogenous arachidonic acid to hydroxy-5,8,10-heptadecatrienoic acid, and TXB2) were higher in smokers than nonsmokers at baseline conditions, immediately and 6 hours after passive exposure to cigarette smoke. Repeated exposure of nonsmokers rendered their platelets more activated, so they became closer to the behavior of smokers. Contributing to the development of hemostatic imbalance, these results indicate that passive smoking may enhance thromboxane A2 release from the platelets.Presented at the 36th Annual World Congress, International College of Angiology, New York, New York, July 1994 |
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