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Low‐dose aspirin does not lower in vivo platelet activation in healthy smokers
Author(s) -
Thomas Pernerstorfer,
Petra Stohlawetz,
Georg Stummvoll,
Stylianos Kapiotis,
Thomas Szekeres,
Eichler Hg,
Bernd Jilma
Publication year - 1998
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1998.00883.x
Subject(s) - platelet , aspirin , platelet activation , p selectin , thromboxane b2 , medicine , thromboxane , endocrinology , placebo , in vivo , pharmacology , biology , pathology , alternative medicine , microbiology and biotechnology
Smoking causes atherosclerosis, and smokers have increased thromboxane (TXA 2 ) formation. As aspirin inhibits TXA 2 production we speculated that smokers would preferentially profit from inhibition of the TXA 2 pathway by aspirin. Increased expression of P‐selectin, a constituent of the alpha‐granules of platelets, and increased levels of circulating (c)P‐selectin in plasma are markers for platelet activation. The aim of this study was to compare P‐selectin expression on platelets between smokers and nonsmokers, and to compare with placebo the effect of 2 weeks administration of 100 mg/d aspirin on platelet activation in smokers. Smokers exhibited higher P‐selectin expression on platelets than non‐smokers (2.7 ± 1.8% v 1.6 ± 0.6%, P = 0.018), thus confirming increased platelet activation. Aspirin did not reduce platelet activation as demonstrated by unchanged P‐selectin expression on platelets and cP‐selectin plasma levels.