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European Journal of Cardio-Thoracic Surgery, Vol 8, 87-90, Copyright © 1994 by European Association for Cardio-thoracic Surgery
N Tabuchi, J De Haan, PW Boonstra, RC Huet and W van Oeveren
A variety of studies have been performed on the preservation of hemostasis
by aprotinin during cardiopulmonary bypass (CPB). It appears that the
mechanism of aprotinin to preserve hemostasis can be interpreted in
different ways. Our previous studies suggested that preservation of
platelet glycoprotein Ib (GpIb) antigen, and counteraction of heparin
anticoagulation in the extrinsic clotting pathway might partly explain the
preservative effect of aprotinin. A clinical study was therefore conducted
to evaluate these effects during the use of low dose aprotinin. Improved
agglutination by ristocetin (P < 0.05), and improved GpIb antigen
expression (P < 0.05) during CPB showed better preserved platelet
adhesive capacity in the aprotinin group than in the control group.
Glycoprotein Ib antigen expression and the agglutination capacity with
ristocetin during CPB were closely related (P < 0.05). Platelet
GpIIb/IIIa antigen and adenosine diphosphate (ADP) aggregation were not
significantly different between the aprotinin and control groups. Aprotinin
had no effect on the extrinsic clotting pathway in the blood, since the
thromboplastin clotting time was similar in both groups. These results
indicate that the protection of platelet adhesive capacity during CPB is a
main function of aprotinin, whereas no evidence was collected for enhanced
extrinsic clotting by aprotinin during CPB.
ARTICLES
Aprotinin effect on platelet function and clotting during cardiopulmonary bypass
Thoraxcenter, Cardiopulmonary Surgery, University Hospital Groningen, The Netherlands.
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