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Gewählte Publikation:

Schmid, P; Karanikas, G; Kritz, H; Pirich, C; Stamatopoulos, Y; Peskar, BA; Sinzinger, H.
Passive smoking and platelet thromboxane.
Thromb Res. 1996; 81(4):451-460 Doi: 10.1016/0049-3848(96)00017-5
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Co-Autor*innen der Med Uni Graz
Peskar Bernhard
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Abstract:
While active smoking is known to enhance platelet thromboxane production, no data on passive smoking is available yet. The influence of single and repeated exposure to passive smoke for 60 minutes in a 18 m3 room was assessed in non-smokers as compared to sex and age matched smokers. All the evaluated measures (malondialdehyde, plasma thromboxane B2, 11-dehydro-thromboxane B2, serum thromboxane B2, conversion of exogenous arachidonic acid to thromboxane B2 and to hydroxy-5, 8,10-heptadecatrienoic acid) were higher in smokers than non-smokers at baseline, immediately and 6 hours after passive exposure to cigarette smoke. Repeated exposure of non-smokers rendered their platelets more activated becoming close to the behaviour of smokers. These results indicate that passive smoking may activate thromboxane A2 release from the platelets, contributing to the development of hemostatic imbalance.
Find related publications in this database (using NLM MeSH Indexing)
Adult -
Blood Platelets - metabolism
Female - metabolism
Humans - metabolism
Male - metabolism
Malondialdehyde - blood
Platelet Function Tests - blood
Thromboxane A2 - blood
Thromboxane B2 - blood
Tobacco Smoke Pollution - adverse effects

Find related publications in this database (Keywords)
passive smoking
platelet thromboxane
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