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Bepridil protects sickle cells against the adverse rheological effects of cyclical deoxygenation
Author(s) -
Johnston M. N.,
Ellory J. C.,
Stuart J.
Publication year - 1989
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1989.tb00291.x
Subject(s) - bepridil , deoxygenation , chemistry , pharmacology , calcium , hemoglobinopathy , medicine , biochemistry , hemolytic anemia , verapamil , catalysis
Summary Calcium influx into sickle cells, with consequential activation of the Ca 2+ ‐activated K + efflux (Gardos) channel, is a potential cause of cellular dehydration and loss of deformability. Bepridil, a recently described inhibitor of the Gardos channel, was found at pharmacological concentration (1 μmol/1) to inhibit significantly (P<0.01) the loss of deformability when sickle cells were subjected to cycles of oxygenation‐deoxygenation for 15 h at 37°C. Bepridil also inhibited significantly ( P < 0.005) the formation of irreversibly sickled cells. Drugs that preserve the K + and therefore water content of erythrocytes are of potential value for hydrotherapy of sickle cell disease.