Inhibition of ristocetin-induced platelet agglutination by vancomycin
JL Moake, PL Cimo, DM Peterson, P Roper and EA Natelson
Ristocetin and vancomycin are structurally similar glycopeptide
antibiotics. Both vancomycin and ristocetin in high concentrations (3.0
mg/ml) cause the precipitation of fibrinogen, plasminogen, and IgG from
platelet-poor plasma (PPP). In contrast to ristocetin, vanomycin (0.5- 1.5
mg/ml) does not agglutinate platelets in normal platelet-rich plasma (PRP)
or formalin-treated platelets in the presence of normal PPP. Preincubation
of vancomycin (0.5-1.25 mg/ml) with normal PRP, von Willebrand platelets in
normal PPP, or formalinized platelets results in inhibition of platelet
agglutination induced by ristocetin (0.7-1.25 mg/ml) or ristocetin and
normal PPP. This inhibition can be overcome by increasing the final
concentration of ristocetin in the platelet suspension. Preincubation of
formalin-treated platelets with the major fraction obtained by
carboxymethyl-Sephadex C-50 chromatography of commercial vancomycin also
results in inhibition of agglutination induced by ristocetin and normal
PPP. Incubation with vancomycin (1.25 mg/ml) does not interfere with von
Willebrand factor (vWF) or factor VIII coagulant activities in normal PPP
or in Sepharose 4B void volume fractions of PPP. These results indicate
that vancomycin interacts with normal, von Willebrand, and formalin-treated
platelets and inhibits the binding of ristocetin (or ristocetin-vWF
complexes).
Volume 50,
Issue 3,
pp. 397-406,
09/01/1977
Copyright © 1977 by The American Society of Hematology
