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  • Title: Decreased platelet adhesion on vessel segments in von Willebrand's disease: a defect in initial platelet attachment.
    Author: Turitto VT, Weiss HJ, Baumgartner HR.
    Journal: J Lab Clin Med; 1983 Oct; 102(4):551-64. PubMed ID: 6413629.
    Abstract:
    The adhesion of platelets to subendothelium exposed to flowing blood involves two distinct morphological stages: (1) platelet contact (C), the initial attachment of unspread, discoid platelets to the subendothelium, and (2) spread platelets (S), the attachment that results as contact platelets spread on the surface and become more firmly bound to it. A defect in either initial platelet attachment or platelet spreading can result in reduced levels of platelet adhesion (C + S). The combined observation of decreased platelet adhesion (C + S) and increased platelet contact (C) has been previously utilized to conclude that a defect exists in the ability of platelets to spread on subendothelium in von Willebrand's disease. In this present investigation, we demonstrate, by modeling the contact and spreading stages of platelet adhesion as a classic set of reactions in series, that the combination of reduced adhesion (C + S) and increased contact (C) is inconclusive with regard to the nature of the adhesion defect in von Willebrand's disease. Decreased adhesion (C + S) coupled with increased platelet contact (C) can result from either decreased rates of initial attachment or decreased rates of spreading. In fact, given the complexity of the temporal behavior of platelet contact (C) and platelet spreading (S), and the relatively small fraction (less than 10%) of the platelets that are in contact (C) at any time, we conclude that a determination of the nature of the adhesion (C + S) defect in von Willebrand's disease is not statistically feasible under conditions in which both contact and spreading occur simultaneously. Experiments were conducted in which blood anticoagulated with EDTA was exposed to subendothelium digested with alpha-chymotrypsin for periods of 10 and 40 min. Under such conditions, platelet spreading (S) was substantially inhibited so that the predominant platelet interaction (greater than 80%) on the subendothelium was platelet contact (C). Values of platelet adhesion (C + S) in von Willebrand's disease were significantly reduced (p less than 0.05) compared with normal values at both exposure times. Thus we conclude that the defect in platelet adhesion (C + S) in von Willebrand's disease appears to be associated with a reduced ability of platelets to attach to the surface rather than their inability to spread on the surface.
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