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Membrane expansion as a mechanism explaining the antisickling action of ticlopidine observed in vitro
Author(s) -
Sablayrolles Magali,
Wajcman Henri,
Castaigne JenaPaul,
Labie Dominique
Publication year - 1985
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830180203
Subject(s) - mechanism of action , ticlopidine , in vitro , mechanism (biology) , pharmacology , action (physics) , chemistry , medicine , biochemistry , philosophy , epistemology , physics , aspirin , clopidogrel , quantum mechanics
Ticlopidine, a platelet antiaggregant, has shown some efficacity in a clinical trial in patients with sickle cell disease. We have studied this agent in vitro to evaluate its effects on sickle erythrocyte. Ticlopidine effects sickling in vitro not by direct interaction with hemoglobin, but via strong binding to the red cell membrane. The density of the whole cell population is decreased when cells are treated with 0.1 mM ticlopidine, which is higher than the concentrations of 1 μM potentially achievable in vivo. Since hemoglobin concentration influences the delay time for gelling, its decrease in the red cell could have a beneficial effect. Such a partial inhibition of the polymerization is shown by oxygen equilibrium studies at various ionic strengths.