AJP - Heart and Circulatory Physiology, Vol 252, Issue 3 615-H621, Copyright © 1987 by American Physiological Society
Fibrinogen receptors in platelet adhesion to surfaces of extracorporeal circuit
P. Gluszko, B. Rucinski, J. Musial, R. K. Wenger, A. H. Schmaier, R. W. Colman, L. H. Edmunds Jr and S. Niewiarowski
The role of platelet fibrinogen receptors and platelet-protein interaction
in platelet consumption during simulated cardiopulmonary bypass was
investigated. In five recirculation experiments, with whole blood, the
platelet count fell to 13% of initial values and in two experiments, with
blood from patients with Bernard-Soulier syndrome, to 3% of normal values.
However, in three experiments with blood from the patients with Glanzmann's
thrombasthenia, the platelet count decreased to 69% of initial values. The
extent of platelet consumption in normal blood was diminished to only 72%
by addition of 0.5 microM prostaglandin E1 (PGE1) (5 experiments) and to
80% by precoating surfaces of the circuit with 2.5% human albumin (5
experiments). beta-Thromboglobulin antigen (beta TG) loss from platelets
was associated with thrombocytopenia. The extent of beta TG loss was
significantly reduced by the addition of PGE1 to blood or precoating
surfaces with albumin. Proteins adsorbed on the surface of the circuit
exposed to normal blood were removed with 0.5% Triton X-100. Some of these
proteins were identified to be glycoprotein IIIa (GPIIIa) (3.4-4.3
micrograms/ml), beta TG (1.0-1.6 micrograms/ml), and fibrinogen (1.9-3.7
micrograms/ml). The amount of GPIIIa recovered in the Triton X-100 eluates
correlated with the number of platelets lost during recirculation. These
studies indicate that exposure of fibrinogen receptors associated with
GPIIb-GPIIIa complex contributes to platelet consumption during
cardiopulmonary bypass.
