Selective thromboxane inhibition: a new approach to antiplatelet therapy. | Zendy

M. Fisher | Zendy; Bonnie H. Weiner | Zendy; Ira S. Ockene | Zendy; J S Hoogasian | Zendy; A M Natale | Zendy; Jeremy Arsenault | Zendy; Martin H. Johnson | Zendy; Peter H. Levine | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Selective thromboxane inhibition: a new approach to antiplatelet therapy.

Author(s) -

M. Fisher,

Bonnie H. Weiner,

Ira S. Ockene,

J S Hoogasian,

A M Natale,

Jeremy Arsenault,

Martin H. Johnson,

Peter H. Levine

Publication year - 1984

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/01.str.15.5.813

Subject(s) - medicine , prostacyclin , aspirin , thromboxane , platelet , pharmacology , thromboxane a2 , platelet aggregation inhibitor , thromboxane a synthase , ex vivo , drug , platelet aggregation , thromboxane receptor , in vivo , microbiology and biotechnology , biology

Antiplatelet drugs as exemplified by aspirin are used frequently to prevent stroke. Aspirin inhibits the formation of both the potent platelet aggregator, thromboxane A2 and the potent anti-aggregator, prostacyclin. Another approach to the inhibition of platelet aggregation might involve selective suppression of thromboxane formation. We report our experience in swine with UK-38,485, a drug which selectively inhibits thromboxane formation. The rationale and potential uses of UK-38,485 in the in vivo prevention of platelet aggregation and for the therapy of cerebrovascular disease are discussed.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research