Multiplate® COLtest

Multiplate® COLtest frontview

Multiplate COLtest

Assay for the quantitative in vitro determination of platelet function triggered by collagen. Following binding of collagen to its receptors, arachidonic acid is released, which is the substrate of the platelet enzyme cyclooxygenase. Cyclooxygenase transforms arachidonic acid into thromboxane A2, a potent platelet activator.Assay for the quantitative in vitro determination of platelet function triggered by TRAP-6. Thrombin receptor activating peptide-6 (TRAP-6) is a potent platelet activator and stimulates platelet aggregation via the thrombin receptor PAR-1.


Collagen is a protein found in the connective tissue of humans. Upon injury to connective tissue such as the skin or a blood vessel, collagen becomes exposed and freely circulating platelets immediately attach themselves to the collagen by means of their glycoprotein VI membrane receptors. Upon attachment, the platelets undergo shape change, membrane release of arachidonic acid, an increase in cytoplasmic calcium, and release of products such as ADP and serotonin from their granules. The presence of ADP and mobilized calcium causes activation of the glycoprotein IIb/IIIa (GPIIb/IIIa) receptor complex culminating in platelet-to-platelet aggregation by means of fibrinogen bridges. Because final collagen induced platelet aggregation is a compilation of collagen, thromboxane, and ADP activated platelets resulting in GPIIb/IIIa mediated aggregation, the influences of substances that inhibit any of these modes of platelet activation and subsequent aggregation may be detectable depending on the concentration of collagen present. Examples of substances or disorders that may reduce or eliminate collagen induced platelet aggregation are: acetylsalicylic acid (cyclooxygenase inhibition), GPIIb/IIIa antagonists and Glanzmann thrombasthenia (deficiency of GpIIb/IIIa receptors).1,2,3,4,5


  1. Pulcinelli, F.M., Pignatelli, P., Celestini, A., et al. (2004). Inhibition of platelet aggregation by acetylsalicylic acid progressively decreases in long-term treated patients. J Am Coll Cardiol.; 43:979-984.
  2. Storey, R.F., Wilcox, R.G., Heptinstall, S. (1998). Differential Effects of Glycoprotein IIb/IIIa Antagonists on Platelet Microaggregate and Macroaggregate Formation and Effect of Anticoagulant on Antagonist Potency. Circulation.;98: 1616-1621.
  3. Moshfegh, K., Redondo, M,. Julmy, F. et al. (2000). Antiplatelet effects of clopidogrel compared with acetylsalicylic acid after myocardial infarction: enhanced inhibitory effects of combination therapy. J Am Coll Cardiol.; 36: 699-705.
  4. Awidi, A., Maqablah, A., Dweik, M., et al. (2009). Comparison of platelet aggregation using light transmission and multiple electrode aggregometry in Glanzmann thrombasthenia. Platelets, August; 20(5): 297-301.
  5. Halimeh, S., Angelis, G., Sander, A., et al. (2010). Multiplate whole blood impedance point of care aggregometry: preliminary reference values in healthy infants, children and adolescents. Klin Padiatr May; 222(3):158-63.

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