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Ann Thorac Surg 1996;61:1188-1193
© 1996 The Society of Thoracic Surgeons
Departments of Thoracic and Cardiovascular Surgery and Pathology, Loyola University Medical Center, Maywood, Illinois
Accepted for publication December 13, 1995.
Background. Aprotinin significantly decreases postoperative blood loss, yet its exact mechanism of action remains unproven.
Methods. To study the cytoprotective effect on platelets, we collected blood samples from patients during cardiopulmonary bypass (CPB) operations performed with or without aprotinin. Analysis included whole-blood flow cytometry.
Results. The highest percentages of activated platelets (positive for GMP-140 expression) were bound to leukocytes and erythrocytes in all CPB patients. Platelet-platelet activation did not reveal any marked differences between groups. However, in the platelet-cell bound region, increased ristocetin-stimulated platelet activation was observed from 30 minutes on CPB to 90 minutes after CPB with aprotinin (11.9% ± 5.1% to 33.1% ± 8.6%; p< 0.05), but not without aprotinin (17.5% ± 0.1% to 17.9% ± 2.3%). Platelet autoactivation increased more in the untreated group with time on CPB.
Conclusions. This study demonstrates that in the presence of aprotinin, platelets remain unstimulated during CPB and the von Willebrand GPIb-mediated activatability of platelets is preserved, thus maintaining a viable platelet population. Most important, this study reveals that these mechanisms are more related to platelet-leukocyte than to platelet-platelet interactions.
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