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Platelet Function in Thrombosis and Atherosclerosis

  • Robert W. Colman
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 104)

Abstract

Thrombosis, frequently the final event in coronary or cerebral arterial occlusion, is a result of the interplay of abnormalities of the arterial intima, hemodynamic stresses, plasma coagulant proteins and platelets. Platelets initiate a series of intricate reactions by adhering to the injured arterial lining, aggregating to form a platelet plug (1) and releasing vasoactive metabolites and hydrolytic enzymes that might in turn alter both the function and structure of the vessel. Heightened platelet function thus might not only participate in the formation of thrombi but may also play a role in the development of progression of some forms of atherosclerosis. Two blood components which may be implicated in atherosclerosis are plasma lipoproteins and platelets. Epidemiologic evidence points to hyperbetalipoproteinemia as an important risk factor in coronary and cerebral arterial occlusion (2). Over the past five years, our laboratory has been gathering clinical and experimental evidence that the plasma lipoprotein composition may influence platelet reactivity by altering either the lipid composition directly or being associated with critical changes in the cholesterol/phospholipid ratio. Membrane protein function may change in an altered lipid environment. Investigations also suggest that lipid soluble drugs such as clofibrate and halofenate can reverse the increased platelet sensitivity probably through altering membrane lipid structure by inducing a phase separation.

Keywords

Platelet Function Platelet Membrane Normal Platelet Induce Phase Separation Lipid Soluble Drug 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    French, J.E. (1971) Semin. Hematol. 8, 84–94.PubMedGoogle Scholar
  2. 2.
    Kannel, W.B., Castelli, W.P., and McNamara, P.M. (1967) J. Occup. Med. 9, 611–621.Google Scholar
  3. 3.
    Carvalho, A.C.A., Colman, R.W., and Lees, R.S. (1974) N. Engl. J. Med. 290, 434–348.PubMedCrossRefGoogle Scholar
  4. 4.
    Cooper, R.A., Arner, E.C., Wiley, J.S., and Shattil, S.J. (1975) J. Clin. Invest. 55, 115–126.PubMedCrossRefGoogle Scholar
  5. 5.
    Shattil, S.J., Bennett, J.S., Colman, R.W., and Cooper, R.A. (1977) J. Lab. Clin. Med. 89, 341–353.Google Scholar
  6. 6.
    Shattil, S.J., Anaya-Galindo, R., Bennett, J., Colman, R.W., and Cooper, R.A. (1975) J. Clin. Invest. 55, 636–643.PubMedCrossRefGoogle Scholar
  7. 7.
    Shattil, S.J., and Cooper, R.A. (1976) Biochemistry 15, 4832–4837.PubMedCrossRefGoogle Scholar
  8. 8.
    Sinha, A.K., Shattil, S.J., and Colman, R.W. (1977) J. Biol. Chem. 252, 3310–3314.PubMedGoogle Scholar
  9. 9.
    Carvalho, A.C.A., Colman, R.W., and Lees, R.S. (1974) Circulation 50, 570–574.PubMedCrossRefGoogle Scholar
  10. 10.
    Colman, R.W., Bennett, J.S., Sheridan, J.F., Cooper, R.A., and Shattil, S.J. (1976) J. Lab. Clin. Med. 88, 282–291.PubMedGoogle Scholar
  11. 11.
    Favis, G.R., and Colman, R.W. (1977) Thromb. and Hemostasis 38, 64.Google Scholar
  12. 12.
    Colman, R.W., Kuchibhotla, J., Jain, M.K., and Murray, R.K., Jr. (1977) Biochem. Biophys. Acta 467, 273–279.CrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1978

Authors and Affiliations

  • Robert W. Colman
    • 1
  1. 1.Coagulation Unit, Hematology-Oncology Section, Department of MedicineUniversity of Pennsylvania Medical SchoolPhiladelphiaUSA

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