Studies on the vasoocclusive crisis of sickle cell disease. III. In vitro and in vivo effect of the pyrimido-pyrimidine derivative, RA-233: studies on its mechanism of action

J Med. 1987;18(3-4):165-98.

Abstract

Red cell deformability was found to be impaired in SS- and SC-genotype and to a lesser extent SA-genotype red blood cells as compared with those of AA-genotype. RA-233 in vitro improved deformability according to a bell-shaped dose-response curve. RA-233 also prevented experimental vasoocclusive crisis in Macaca arctoides. Deoxygenation of SS-genotype red cells resulted in sickle shape transformation, ATP depletion, potassium efflux, and attachment of hemoglobin molecules to the membrane. These changes were prevented by RA-233. Suspending SS-genotype red blood cells in potassium rich tris-buffer also prevented potassium efflux during deoxygenation and also decreased cellular deformability. RA-233 had no effect on osmotic fragility of SS-genotype red blood cells.

MeSH terms

  • Adult
  • Anemia, Sickle Cell / blood
  • Anemia, Sickle Cell / drug therapy*
  • Animals
  • Antisickling Agents / pharmacology
  • Antisickling Agents / therapeutic use*
  • Child
  • Child, Preschool
  • Erythrocyte Deformability / drug effects
  • Female
  • Genotype
  • Humans
  • Macaca
  • Male
  • Mopidamol / pharmacology
  • Mopidamol / therapeutic use*
  • Osmotic Fragility / drug effects
  • Platelet Aggregation / drug effects
  • Potassium / metabolism
  • Pyrimidines / therapeutic use*

Substances

  • Antisickling Agents
  • Pyrimidines
  • Mopidamol
  • Potassium