Thromb Haemost 1983; 50(03): 703-706
DOI: 10.1055/s-0038-1665291
Original Article
Schattauer GmbH Stuttgart

The Effect of a Thromboxane Synthetase Inhibitor, Dazoxiben, and Acetylsalicylic Acid on Platelet Function and Prostaglandin Metabolism

Jon Dale
The Medical Department B, Research Institute for Internal Medicine, Rikshospitalet, Oslo, Norway, and Pfizer Central Research, Pfizer Ltd., Sandwich, Kent, England
,
Erik Thaulow
The Medical Department B, Research Institute for Internal Medicine, Rikshospitalet, Oslo, Norway, and Pfizer Central Research, Pfizer Ltd., Sandwich, Kent, England
,
Erik Myhre
The Medical Department B, Research Institute for Internal Medicine, Rikshospitalet, Oslo, Norway, and Pfizer Central Research, Pfizer Ltd., Sandwich, Kent, England
,
John Parry
The Medical Department B, Research Institute for Internal Medicine, Rikshospitalet, Oslo, Norway, and Pfizer Central Research, Pfizer Ltd., Sandwich, Kent, England
› Author Affiliations
Further Information

Publication History

Received 03 December 1982

Accepted 27 July 1983

Publication Date:
18 July 2018 (online)

Summary

Twenty-four men received either placebo, 0.1 g of the thromboxane synthetase inhibitor dazoxiben, 0.25 or 1.0 g of acetylsalicylic acid (ASA). Dazoxiben reduced the maximal rate of collagen-induced platelet aggregation, but less than did ASA. ASA abolished secondary, ADP-induced aggregation, dazoxiben not. Both drugs prolonged the bleeding-time.

Plasma thromboxane B2 (TxB2) levels did not change significantly after dazoxiben, whereas the prostacyclin metabolite 6-keto-PGF rose. The larger dose of ASA reduced both TxB2 and 6-keto-PGF in plasma. Whole blood was allowed to clot in order to estimate prostaglandin metabolism. Both drugs prevented thromboxane production effectively. Formation of 6-keto-PGF decreased by 95 per cent after ASA but was more than doubled after dazoxiben.

Dazoxiben is a selective and effective thromboxane synthetase inhibitor, but has a weaker effect on platelet reactivity than ASA, possibly because endoperoxide formation is not prevented.

 
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