Effect of red blood cells from patients with sickle cell disease on platelet factor 3 release.
Red cells from two SS genotype and two SA genotype patients were sampled. When the samples were deoxygenated and mixed with platelet-rich plasma, they caused the release of platelet factor 3 as recorded in a coagulometer. This phenomenon was not present in control blood samples from normal individuals. Membrane changes in abnormal red cells during hypoxia may be responsible in part for platelet activation and its role in vasoocclusive crisis. Vasoocclusive crisis could be prevented by increasing the red cell membrane fluidity and inhibiting the platelet aggregation with pentoxifylline.
Toumbis
C A
CA
Department of Medicine, Roswell Park Cancer Institute, State University of New York, Buffalo.
Stadler
I
I
Ambrus
J L
JL
D000328:Adult; D000755:Anemia, Sickle Cell / Q000097:blood* / Q000235:genetics; D004912:Erythrocytes / Q000473:pathology / Q000502:physiology*; D005838:Genotype; D006801:Humans; D008297:Male; D010431:Pentoxifylline / Q000494:pharmacology; D015539:Platelet Activation / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D010977:Platelet Factor 3 / Q000378:metabolism*
D010975:Platelet Aggregation Inhibitors; D010977:Platelet Factor 3; D010431:Pentoxifylline