The inability of low-molecular-weight dextran, aspirin, and prostaglandin E1 to inhibit monolayer platelet adhesion to polyethylene.

In aggregometry studies employing platelet-rich plasma, monoclonal antibody 6D1 (6D1) binds to platelet membrane glycoprotein 1b (GP1b) and has been shown to abolish agglutination with ristocetin (1.5 mg/ml), with little effect on first-phase and slight diminution of second-phase aggregation with adenosine diphosphate (20 mumol/L). In perfusion studies with polyethylene microconduits (PE-100; interior diameter, 0.86 mm; length, 5 cm), platelet deposition (platelets/cm2) is restricted to a patchy monolayer when platelets are treated with 6D1 (10 micrograms/ml), providing a new model to study surface platelet adhesion isolated from platelet aggregation. The power of low-molecular-weigh dextran (DEX; mild inhibitor of fibrin formation and polymerization and von Willebrand factor-platelet interaction), aspirin (ASA; cyclooxygenase inhibitor), and prostaglandin E1 (PGE1; adenylate cyclase stimulator) to inhibit platelet adhesion on PE-100 was tested with this model. PE-100 segments were perfused with citrated human blood (5 ml, hematocrit, 35% +/- 5%) containing 6D1-treated, 111indium (111In-)labeled platelets (2.0 +/- 0.5 x 10(5) platelets/microliters) in a customized perfusion chamber (37 degrees C; flow, 1.2 ml/min; shear, 312 s-1). After a buffer flush under the same conditions, platelet deposition was measured by 111In-scintigraphy of the perfused conduits.(ABSTRACT TRUNCATED AT 250 WORDS)