The inability of low-molecular-weight dextran, aspirin, and prostaglandin E1 to inhibit monolayer platelet adhesion to polyethylene
Garrett, K.O.; Pautler, S.V.; Johnson, P.C.
Journal of Laboratory and Clinical Medicine 122(2): 141-148
1993
ISSN/ISBN: 0022-2143 PMID: 7688020 Document Number: 405796
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 mu-mol/L). In perfusion studies with polyethylene microconduits (PE-100; interior diameter, 0.86 mm; length, 5 cm), platelet deposition (platelets/cm-2) is restricted to a patchy monolayer when platelets are treated with 6D1 (10 mu-g/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 E-1 (PGE-1; 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 times 10-5 platelets/mu-l) in a customized perfusion chamber (37 degree 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. When no 6D1 was present, platelet deposition was 5.48 +- 1.91 times greater (mean +- SD, n = 12) than when platelets were treated with 6D1 alone (1.00 +- 0.25, n = 43, p lt 0.001, analysis of variance), and no further reduction in platelet adhesion resulted from addition of DEX, 4 mg/ml (0.99 +- 0.73, p = 0.98, n = 13), ASA, 5 mmol/L (1.12 +- 0.63, p = 0.74, n = 13), or PGE-1, 1 mu-mmol/L (0.63 =0.54, p = 0.34, n = 13) to 6D1-treated platelets. Scanning electron microscopy demonstrated a patchy monolayer of platelets In the groups treated with 6D1 and multilayer platelet deposition In the absence of 6D1. These data, obtained under circumstances that allow assessment of platelet adhesion alone, suggest that DEX, ASA, and PGE-1 do not inhibit platelet adhesion on polyethylene.