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Platelet Adherence to the Vessel Wall and to Collagen-Coated Surfaces

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Thrombosis

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 102))

Abstract

A rotating probe system has been developed to quantitate the adherence of 51Cr-labeled platelets to collagen-coated glass rods or to the subendothelium of the rabbit aorta. The platelets were suspended in a medium containing physiological concentrations of calcium and magnesium, albumin, and apyrase to prevent aggregation. Chelation of divalent cations in the medium by addition of sodium citrate, EDTA, or EGTA markedly diminished platelet adherence. These observations indicate that the interpretation of platelet adherence studies performed in the presence of these agents is questionable. Increasing albumin concentrations in the medium decreased the number of adherent platelets, whereas increasing the hematocrit increased platelet adherence. Thus the factors influencing platelet adherence were studied in the presence of 4% albumin and 40% hematocrit.

When the platelet surface was modified by treatment with thrombin, plasmin, trypsin, chymotrypsin, or ADP, platelet adherence to the surfaces was decreased. Removal of surface sialic acid by neuraminidase had no effect on adherence. Exposing the endothelial surface of an aorta to thrombin resulted in a marked increase in platelet adherence to the thrombin-treated surface; this effect was prevented by adding heparin to the platelet suspension. Platelet adherence to collagen and to subendothelium was inhibited by several drugs that are used in man: dipyridamole, RA 433, methylprednisolone, and the antibiotics penicillin G and cephalothin. Under the experimental conditions used, ASA did not inhibit adherence to collagen, although indomethacin and a high concentration of sulfinpyrazone did. None of these three drugs inhibited release of granule contents from the adherent platelets. Therefore, it is unlikely that they would inhibit smooth muscle proliferation in response to the platelet growth factor released from platelets adherent to collagen in the subendothelium at a site of vessel wall injury.

This work was supported by Medical Research Council of Canada Grants MT 1309 and MT 2629 and by Senior Research Fellowships of the Ontario Heart Foundation to J.-P. Cazenave and R. L. KinloughRathbone.

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Author information

Authors and Affiliations

  1. Department of Pathology, McMaster University, Hamilton, Ontario, Canada

    Jean-Pierre Cazenave M.D.,Ph.D., Marian A. Packham Ph.D., Raelene L. Kinlough-Rathbone M.D.,Ph.D. & J. Fraser Mustard M.D.,Ph.D.

  2. Department of Biochemistry, University of Toronto, Ontario, Canada

    Jean-Pierre Cazenave M.D.,Ph.D., Marian A. Packham Ph.D., Raelene L. Kinlough-Rathbone M.D.,Ph.D. & J. Fraser Mustard M.D.,Ph.D.

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  1. Jean-Pierre Cazenave M.D.,Ph.D.
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  2. Marian A. Packham Ph.D.
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  3. Raelene L. Kinlough-Rathbone M.D.,Ph.D.
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  4. J. Fraser Mustard M.D.,Ph.D.
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Editors and Affiliations

  1. Department of Medicine, Section of Hematology, Temple University, Health Sciences Center, 19140, Philadelphia, PA, USA

    H. James Day M.D.

  2. Diabetes and Atherosclerosis Research, The Upjohn Company, 49001, Kalamazoo, MI, USA

    Basil A. Molony M.D. , Edward E. Nishizawa Ph.D.  & Ronald H. Rynbrandt Ph.D. ,  & 

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Cazenave, JP., Packham, M.A., Kinlough-Rathbone, R.L., Mustard, J.F. (1978). Platelet Adherence to the Vessel Wall and to Collagen-Coated Surfaces. In: Day, H.J., Molony, B.A., Nishizawa, E.E., Rynbrandt, R.H. (eds) Thrombosis. Advances in Experimental Medicine and Biology, vol 102. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-1217-9_3

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  • DOI: https://doi.org/10.1007/978-1-4757-1217-9_3

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