Affiliation:
1. From the Department of Medicine and Center of Excellence on Aging, G. d’Annunzio University, School of Medicine, and G. d’Annunzio University Foundation, Chieti (M.L.C., S.T., M.G.S., M.G., E.R., C.P., P.P.); the Department of Pharmacology, University of Rome La Sapienza (C.P.); SS. Annunziata Hospital, Chieti (P.D., G.M.); and the Department of Biomedical and Surgical Sciences, University of Verona (P.M.), Italy.
Abstract
Background—
The current controversy on the potential cardioprotective effect of naproxen prompted us to evaluate the extent and duration of platelet, monocyte, and vascular cyclooxygenase (COX) inhibition by naproxen compared with low-dose aspirin.
Methods and Results—
We performed a crossover, open-label study of low-dose aspirin (100 mg/d) or naproxen (500 mg BID) administered to 9 healthy subjects for 6 days. The effects on thromboxane (TX) and prostacyclin biosynthesis were assessed up to 24 hours after oral dosing. Serum TXB
2
, plasma prostaglandin (PG) E
2
, and urinary 11-dehydro-TXB
2
and 2,3-dinor-6-keto-PGF
1α
were measured by previously validated radioimmunoassays. The administration of naproxen or aspirin caused a similar suppression of whole-blood TXB
2
production, an index of platelet COX-1 activity ex vivo, by 94±3% and 99±0.3% (mean±SD), respectively, and of the urinary excretion of 11-dehydro-TXB
2
, an index of systemic biosynthesis of TXA
2
in vivo, by 85±8% and 78±7%, respectively, that persisted throughout the dosing interval. Naproxen, in contrast to aspirin, significantly reduced systemic prostacyclin biosynthesis by 77±19%, consistent with differential inhibition of monocyte COX-2 activity measured ex vivo.
Conclusions—
The regular administration of naproxen 500 mg BID can mimic the antiplatelet COX-1 effect of low-dose aspirin. Naproxen, unlike aspirin, decreased prostacyclin biosynthesis in vivo.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine
Cited by
201 articles.
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