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In vivo platelet aggregation in the rat: dependence on extracellular divalent cation and inhibition by nonsteroidal anti‐inflammatory drugs
Author(s) -
Mallarkey G.,
Smith G.M.
Publication year - 1984
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1984.tb10740.x
Subject(s) - chemistry , in vivo , divalent , extracellular , pharmacology , nonsteroidal , platelet , biophysics , platelet aggregation , biochemistry , medicine , biology , microbiology and biotechnology , organic chemistry
1 Using the Technicon Autocounter, the mechanisms involved in collagen‐induced platelet aggregation in vivo have been studied without the interference of an anticoagulant. 2 Extracellular divalent cation was essential for in vivo platelet aggregation. 3 Non‐steroidal anti‐inflammatory drugs completely inhibited the aggregation induced by collagen in platelet‐rich plasma in in vitro or ex vivo studies. In vivo only a maximum of 50% inhibition was achieved when release of thromboxane A 2 (TXA 2 ) was completely inhibited. Therefore in vivo , collagen causes aggregation through more than one pathway which operate independently of each other and which are all dependent on extracellular divalent cation. 4 In vivo , when different doses of collagen were compared, aggregation produced by low doses of collagen was more dependent upon prostaglandin endoperoxide/TXA 2 formation.