Importance of fibrinogen and platelet membrane glycoprotein IIb/IIIa in shear-induced platelet aggregation

Yasuo Ikeda, Mitsuru Murata, Yohko Araki, Kiyoaki Watanabe, Yasuhiko Ando, Ichiro Itagaki, Yuichi Mori, Mayumi Ichitani, Kiyotaka Sakai

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17 Citations (Scopus)


The mechanism of shear-induced platelet aggregation was investigated using a polycarbonate cone and plate viscometer. After exposed to shear stress of 54-90 dyne/cm2 for 2 min. at 37°C, platelets aggregated without a significant amount of serotonin release and lactic dehydrogenase leakage from platelets. Under this conditions, platelets from 2 patients with thrombasthenia and a patient with congenital afibrinogenemia failed to aggregate. When fibrinogen was added to platelet rich plasma from a patient with afibrinogenemia, shear-induced platelet aggregation occurred at the same extent of aggregation as observed in normal platelets. Shear-induced platelet aggregation was inhibited by monoclonal antibody to GPIIb/IIIa (1 μg/ml) and synthetic peptide, Arg-Gly-Asp-Ser (RGDS) (1 mM). Apyrase and hirudin showed no effect on this aggregation. Indomethacin (100 μM) and thromboxane A2 synthetase inhibitor, OKY-046 (100 μM) markedly inhibited aggregation, while thromboxane A2 competitive inhibitor, ONO-3708 (100 μM) exhibited only partial inhibition. These results indicate that fibrinogen and GPIIb/IIIa are important for shear-induced platelet aggregation and that the induction of fibrinogen receptor on GPIIb/IIIa may partially depend upon thromboxane A2 synthesis in platelets.

Original languageEnglish
Pages (from-to)157-163
Number of pages7
JournalThrombosis Research
Issue number2
Publication statusPublished - 1988 Jul 15


  • GPIIb/IIIa
  • fibrinogen
  • shear-induced platelet aggregation

ASJC Scopus subject areas

  • Hematology


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