Open AccessProtection of Platelet Glycoprotein llb/llla Receptor Complex Preserves Platelet Function During In Vitro Ventricular Assisted Circulation
Author(s) -
John C. Chen,
Dan L. Serna,
Lisa Tran,
Joseph Huh,
Lauren Powell,
Bryan O. King,
Rayhan Jalal,
Earl Steward,
Richard Newman
Publication year - 1998
Publication title -
asaio journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.961
H-Index - 66
eISSN - 1538-943X
pISSN - 1058-2916
DOI - 10.1097/00002480-199809000-00076
Subject(s) - ristocetin , platelet , in vitro , fibrinogen , adenosine diphosphate , chemistry , receptor , medicine , platelet membrane glycoprotein , endocrinology , platelet aggregation , biochemistry
Platelet dysfunction probably contributes to bleeding associated with ventricular assist devices (VADs). Previous evidence suggests that VAD associated platelet dysfunction may be due to dysfunction of the platelet fibrinogen receptor. The purpose of this investigation was to test the hypothesis that selective protection of platelet fibrinogen receptor preserves platelet aggregating ability during in vitro ventricular assisted circulation. Eight in vitro nonpulsatile centrifugal VAD circuits were simulated for four days using 450 ml of fresh human whole blood. Temperature, activated clotting time, pH, PCO2, PO2, Ca2+, and glucose were maintained at physiologic values. Flow was maintained at a constant 2.0 L/min/m2. We examined whole blood platelet aggregation induced by ristocetin, collagen, and adenosine diphosphate (ADP). We added a highly specific reversible inhibitor (MK-383) of the glycoprotein (GP) IIb/IIIa receptor complex before start of circulation to the final four VAD experiments. ADP induced aggregation decreased within the first hour of circulation. Ristocetin and collagen induced aggregation decreased to negligible levels after 10 hours of circulation. With MK-383, ristocetin induced aggregation was preserved. Addition of MK-383 did not alter the decrease of ADP and collagen induced aggregation. These results suggest platelet aggregating ability is maintained with protection of the platelet fibrinogen receptor during in vitro ventricular assisted circulation.