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EDTA-induced changes in platelet structure and function: clot retraction.

J G White1

  • 1Department of Laboratory Medicine, University of Minnesota Medical School, Minneapolis 55455, USA.

Platelets
|August 12, 2000
PubMed
Summary
This summary is machine-generated.

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Ethylenediamine tetracetic acid (EDTA) affects blood platelets, yet EDTA-treated platelets still retract clots. This suggests glycoprotein alpha IIb beta 3 (GPIIb/IIIa) receptors may reassociate or be initially inaccessible.

Area of Science:

  • Hematology
  • Biochemistry
  • Cell Biology

Background:

  • Ethylenediamine tetracetic acid (EDTA) is known to cause structural and functional damage to blood platelets.
  • This damage includes irreversible dissociation of the fibrinogen receptor, glycoprotein alpha IIb beta 3 (GPIIb/IIIa).
  • Despite these effects, EDTA-treated platelets can still support clot retraction.

Purpose of the Study:

  • To investigate differences in platelet-fibrin interactions in clots formed from blood collected in EDTA versus citrate.
  • To examine the role of glycoprotein alpha IIb beta 3 (GPIIb/IIIa) in clot retraction of EDTA-treated platelets.

Main Methods:

  • Clot retraction under isometric tension.
  • Electron microscopy.
  • Comparison of clots from blood collected in EDTA and citrate.

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Main Results:

  • No physical differences were identified between clots formed from EDTA or citrate anticoagulated blood.
  • Polymerizing fibrin intimately bound to aggregates of EDTA-treated platelets during clot retraction.
  • Platelets underwent shape change, internal transformation, adhesion, and spreading on fibrin strands.

Conclusions:

  • Glycoprotein alpha IIb beta 3 (GPIIb/IIIa) receptors may reassociate immediately after clot retraction initiation.
  • Alternatively, a significant proportion of GPIIb/IIIa receptors on resting platelets might be inaccessible to EDTA and become available upon thrombin activation.