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The platelet function defect of cardiopulmonary bypass
A S Kestin1, C R Valeri, S F Khuri
1Department of Medicine, Medical Center of Central Massachusetts, Worcester.
Blood
|July 1, 1993
Summary
Cardiopulmonary bypass (CPB) impairs platelet function during cardiac surgery, causing prolonged bleeding. This defect is extrinsic, not intrinsic to platelets, likely due to reduced platelet activators like thrombin during CPB.
Area of Science:
- Cardiovascular Surgery
- Hemostasis and Thrombosis
- Platelet Physiology
Background:
- Cardiopulmonary bypass (CPB) is linked to hemostatic defects and prolonged bleeding times after cardiac surgery.
- The exact nature of the platelet function impairment during CPB remains controversial.
Purpose of the Study:
- To investigate the characteristics of platelet function defects during CPB.
- To differentiate between intrinsic platelet defects and extrinsic factors contributing to impaired hemostasis.
Main Methods:
- Whole-blood flow cytometry was used to analyze platelet surface glycoproteins (GP Ib-IX, GP IIb-IIIa, P-selectin) before, during, and after CPB.
- Platelet reactivity was assessed using in vitro agonists (phorbol myristate acetate, U46619, ADP/epinephrine).
- Plasma glycocalicin and shed-blood thromboxane B2 (TXB2) levels were measured.
Main Results:
- Platelet P-selectin expression in shed blood was reduced during CPB, correlating with prolonged bleeding times and decreased TXB2 generation.
- In vitro platelet reactivity to agonists remained normal during and after CPB.
- No significant changes were observed in platelet surface GP Ib-IX or GP IIb-IIIa expression in peripheral blood.
Conclusions:
- CPB induces a functional platelet defect primarily related to impaired in vivo activation at the wound site, not an intrinsic platelet abnormality.
- The defect appears extrinsic, possibly due to a lack of platelet agonists in vivo.
- Heparin's inhibition of thrombin, a key platelet activator, likely contributes significantly to this hemostatic defect.