Thrombin receptor-related hemostatic defect after cardiopulmonary bypass

Seminars in Thrombosis and Hemostasis
V A FerrarisJ W Fenton

Abstract

Platelet abnormalities have been blamed for the hemostatic defect that develops after cardiopulmonary bypass (CPB), but investigators have not been able to agree upon an intrinsic platelet abnormality responsible for the observed defect. To better define the blood components responsible for this post-operative hemostatic defect, we compared platelet function in whole blood (WB) to that in platelet-rich plasma (PRP) in 33 patients undergoing coronary artery bypass grafting. We measured platelet aggregation in response to various platelet agonists, including thrombin and TRAP-6 (a 6-amino acid peptide that activates the thrombin "tethered ligand" receptor site). In WB there was a lasting, diminished response to TRAP-6, but not to gamma-thrombin, after CPB. Control experiments showed that this diminished response to TRAP-6: (1) was not related to heparin or heparin-protamine complexes, (2) was not the result of hemodilution during CPB, (3) was not related to increased amounts of naturally occurring enzymes (aminopeptidases) that degrade TRAP, and (4) was not able to be reversed by the addition of as much as a 10-fold excess of the usual TRAP-6 aggregating dose to WB preparations. In contrast, no corresponding defect in platelet ag...Continue Reading

Citations

Feb 20, 2003·Thrombosis Research·Marcus E CarrPhilip E Greilich
Jan 24, 2014·British Journal of Haematology·Simon Davidson
May 20, 2015·Journal of Cardiothoracic and Vascular Anesthesia·Seema AgarwalBilal Haneef Kirmani
Mar 4, 1998·The Annals of Thoracic Surgery·V A FerrarisH Reich
Mar 2, 1999·British Journal of Haematology·D H Bevan

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