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Ann Thorac Surg 1997;63:663-668
© 1997 The Society of Thoracic Surgeons
Department of Cardiothoracic Surgery, Killingbeck Hospital, and Research School of Medicine, University of Leeds, Leeds, United Kingdom
Accepted for publication September 30, 1996.
Background. The use of heparin-bonded cardiopulmonary bypass circuits with reduced doses of heparin sodium has been shown to give hemostatic benefits to the patient. However, fears persist that the use of less heparin may put the patient at risk for thrombotic events. This work tested the hypothesis that heparin-bonded circuits per se are effective in preserving cells and reducing thrombin generation when a reduced dose of heparin is used in vitro.
Methods. Simulated extracorporeal circulation was carried out using the same unit of fresh heparinized (1.1 U/mL) human blood to simultaneously perfuse a heparin-bonded circuit and a nonbonded circuit. Samples were taken at 30, 60, 120, and 360 minutes and analyzed for markers of cell activation and thrombin generation.
Results. The concentrations of platelet and white blood cell activation markers were found to be significantly lower in the heparin-bonded circuits compared with the nonbonded circuits. In addition, markers of thrombin generation were significantly lower in bonded circuits. Scanning electron microscopy revealed fewer adherent cells and less debris on the bonded surface compared with the nonbonded surface.
Conclusions. Cell activation and thrombin generation were significantly reduced as a result of the presence of immobilized heparin in a system of cardiopulmonary bypass with reduced plasma heparin. However, evidence of contact activation in the bonded circuits was found after 120 minutes, indicating that anticoagulation in the system was not adequate. This becomes more important clinically where the extrinsic pathway of coagulation is also involved.
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