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Oxidant Stress and Aspirin-Insensitive Thromboxane Biosynthesis in Severe Unstable Angina
Author(s) -
Francesco Cipollone,
Giovanni Ciabattoni,
Paola Patrignani,
Massimo Pasquale,
Domenico Di Gregorio,
Tonino Bucciarelli,
Giovanni Davı̀,
Franco Cuccurullo,
Carlo Patrono
Publication year - 2000
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.102.9.1007
Subject(s) - unstable angina , medicine , aspirin , arachidonic acid , thromboxane b2 , endocrinology , excretion , creatinine , thromboxane a2 , angina , lipid peroxidation , isoprostane , cardiology , ischemia , thromboxane , platelet , oxidative stress , myocardial infarction , biochemistry , chemistry , enzyme
Unstable angina is associated with enhanced lipid peroxidation and reduced antioxidant defenses. We have previously reported aspirin failure in the suppression of enhanced thromboxane (TX) biosynthesis in a subset of episodes of platelet activation in this setting. We tested the hypothesis that the in vivo formation of the F(2)-isoprostane 8-iso-prostaglandin (PG)F(2alpha), a bioactive product of arachidonic acid peroxidation, is enhanced in unstable angina and contributes to aspirin-insensitive TX biosynthesis.

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