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Mechanism and characteristics of platelet activation by haematin
Author(s) -
Neely Sara M.,
Gardner Diane V.,
Reynolds Nancy,
Green David,
Tšao Chunghsin
Publication year - 1984
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1984.tb06089.x
Subject(s) - platelet , chemistry , aspirin , platelet aggregation , divalent , biochemistry , fibrinogen , nucleotide , biophysics , biology , immunology , organic chemistry , gene
Summary The mechanism as well as some characteristics of haematin‐induced human platelet aggregation were investigated. Haematin‐induced platelet aggregation required the presence of devalent cations; Mg 2+ , and to a lesser extent, Co 2+ , were just as effective as Ca 2+ in supporting the aggregation. Mono‐ and trivalent cations were ineffective. Verapamil inhibited the aggregation. The aggregation was accompanied by thromboxane formation which could be abolished by aspirin. The release of adenine nucleotides was only slightly inhibited by aspirin. The rate of aggregation and the ultrastructure of the aggregated platelets were comparable between control and aspirin‐treated samples. It is concluded therefore that haematin‐induced aggregation is not dependent on platelet prosta‐glandin synthesis. Haematin induced binding of fibrinogen to platelets, and failed to aggregate thrombasthenic platelets. These findings indicate that haematin may induce platelet aggregation by promoting influx of divalent cations in association with increased fibrinogen binding and release of adenine nucleotides.