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Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
10:10

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells

Published on: October 26, 2009

Inhibition of in vitro platelet aggregation and release and fibrinolysis

S Narayanan1

  • 1Department of Pathology, New York Medical College-Metropolitan Hospital Center, NY 10029.

Annals of Clinical and Laboratory Science
|July 1, 1989
PubMed

Insights

Accurate platelet activation assessment requires inhibiting in vitro platelet aggregation using additives like CTAD, which is more stable than PGE1-based mixtures. Inhibiting fibrinolysis is crucial for measuring fibrin degradation products, especially with rt-PA therapy.

Area of Science:

  • Hematology
  • Clinical Chemistry
  • Biochemistry

Background:

  • Accurate assessment of in vivo platelet activation requires effective inhibition of in vitro platelet aggregation and granule release.
  • Inhibition of in vitro fibrinolysis is essential for reliable measurement of fibrin degradation products (FDP).

Purpose of the Study:

  • To evaluate practical blood collection additives for inhibiting platelet activation and fibrinolysis for accurate diagnostic testing.
  • To compare the efficacy and stability of different inhibitor mixtures for blood collection.

Main Methods:

  • Investigated citrate, theophylline, adenosine, and dipyridamole (CTAD) as an alternative to acid citrate dextrose (ACD), acetylsalicylic acid (aspirin), and prostaglandin E1 (PGE1) for platelet inhibition.
  • Examined the use of thrombin, soybean trypsin, or aprotinin, supplemented with reptilase for heparinized patients, to inhibit fibrinolysis.
  • Assessed D-phenylalanine-proline-arginine-chloromethylketone (PPACK) as a superior inhibitor for blood collection during recombinant tissue-type plasminogen activator (rt-PA) therapy compared to aprotinin.

Main Results:

  • The CTAD mixture offers a practical alternative to ACD/aspirin/PGE1 due to prostaglandin E1's stability issues.
  • Fibrinolysis inhibitors are necessary for FDP measurement, with reptilase required for heparinized patients.
  • PPACK demonstrates superiority over aprotinin as a blood collection additive inhibitor in the context of rt-PA therapy.

Conclusions:

  • CTAD provides a stable and practical solution for inhibiting platelet activation in vitro.
  • Effective fibrinolysis inhibition strategies are critical for accurate FDP quantification, especially in specific patient populations.
  • PPACK represents an advanced additive for blood collection, particularly beneficial for patients undergoing rt-PA therapy.

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