Int J Angiol 1996; 5(3): 134-139
DOI: 10.1007/BF02043209
Original Articles

© Georg Thieme Verlag KG Stuttgart · New York

Passive smoking increases platelet thromboxane

Harald Kritz1 2 , Peter Schmid4 , Georgios Karanikas3 , Christian Pirich3 , Yannis Stamatopoulos3 , Bernhard A. Peskar5 , Helmut Sinzinger1
  • 1Wilhelm Auerswald Atherosclerosis Research Group, Vienna, Austria
  • 2Rehabilitation Center “Engelsbad-Melanie”, Baden, Lower Austria, Austria
  • 3Department of Nuclear Medicine, University of Vienna, Vienna, Austria
  • 4Cardiovascular Rehabilitation Center Bad Schallerbach, Upper Austria, Austria
  • 5Department of Pharmacology and Toxicology, Ruhr-University, Bochum, Germany
Presented at the 36th Annual World Congress, International College of Angiology, New York, New York, July 1994
Further Information

Publication History

Publication Date:
22 April 2011 (online)

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.

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