Arachidonate induced aggregation of rat platelets may not require prostaglandin endoperoxides or thromboxane A2

Platelet aggregation was measured in rat and human platelet-rich plasma (PRP) after the addition of various amounts of arachidonic acid (AA), prostaglandin H2 (PGH2), adenosine diphosphate (ADP), or collagen. AA but not PGH2 caused rat platelets to aggregate in citrated or heparinized PRP. Both AA a...

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Bibliographic Details
Published inThrombosis research Vol. 30; no. 3; pp. 289 - 296
Main Authors Nishizawa, E E, Williams, D J, Connell, C L
Format Journal Article
LanguageEnglish
Published United States 01.05.1983
Subjects
Animals
Arachidonic Acids - pharmacology
Male
Methacrylates - pharmacology
Platelet Aggregation - drug effects
Prostaglandin Endoperoxides - physiology
Rats
Rats, Inbred Strains
Thromboxane A2 - physiology
Thromboxanes - physiology
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Summary:Platelet aggregation was measured in rat and human platelet-rich plasma (PRP) after the addition of various amounts of arachidonic acid (AA), prostaglandin H2 (PGH2), adenosine diphosphate (ADP), or collagen. AA but not PGH2 caused rat platelets to aggregate in citrated or heparinized PRP. Both AA and PGH2 produced significant amounts of thromboxane A2 (TxA2) measured as thromboxane B2 (TxB2). The lack of aggregation of rat platelets with PGH2 was not due to the formation of an inhibitor of aggregation such as a prostaglandin. Thus, the formation of TxA2 may not be necessary for aggregation of rat platelets. Human platelets were aggregated by PGH2 with the concomitant formation of TxB2.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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ISSN:0049-3848
1879-2472
DOI:10.1016/0049-3848(83)90082-8