The Platelet Function Defect of Cardiopulmonary Bypass.
Abstract
The use of cardiopulmonary bypass (CPB) during cardiac surgery is associated with a hemostatic defect, the hallmark of which is a markedly prolonged bleeding time. However, the nature of the putative platelet function defect is controversial. In this study, blood from 16 patients was collected and analyzed at 10 time points before, during and after CPB. We utilized a whole blood flow cytometric assay to study platelet surface glycoproteins in a) peripheral blood, b) peripheral blood activated in vitro by either phorbol myristate acetate, the thromboxane (TX) A2 analogue U46619, or a combination of adenosine diphosphate and epinephrine, and c) the blood emerging from a bleeding time wound (shed blood). Activation-dependent changes were detected by monoclonal antibodies directed against GPIb, the GPIIb-IIIa complex, and P-selectin. In addition, we measured plasma glycocalicin (a proteolytic fragment of GPIb) and shed blood TXB2 (a stable breakdown product of TXA2). In shed blood emerging from a bleeding time wound, the usual time-dependent increase in platelet surface P-selectin was absent during CPB, but returned to normal within 2 hours. This abnormality paralleled both the CPB-induced prolongation of the bleeding time and a CPB-induced marked reduction in shed blood TXB2 generation.
Document Details
- Document Type
- Technical Report
- Publication Date
- Nov 24, 1992
- Accession Number
- ADA360345
Entities
People
- Anita S. Kestin
- C.r. Valeri
- J. Loscalzo
- P.a. Ellis
- S.f. Khuri
Organizations
- Boston University