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Glycerol-2-3H uptake into phospholipids separated by unidirectional chromatography on silica gel H plates, was measured in normal platelets and those from patients with Glanzman’s thrombasthenia (GT), Bernard-Soulier syndrome (B-S), Storage pool deficiency (SPD) or aspirinlike release defect . The results were compared with the release of adenine nucleotides (AN) and with changes in platelet factor 3 availability (PF3a). In normal platelets, secondary aggregation induced by adenosine diphosphate (ADP), Epinephrine (EPI) , Collagen (COL) or Ristocetin (RI) led to a marked stimulation of glycerol uptake over a 60 minute period of incubation, the most striking increase being in the phosphatidyl inositol (PI) fraction.  No quantitative differences in phospholipid distribution were noted in any of the patients tested. In all cases, the uptake of glycerol was proportional to the degree of platelet aggregation, being minimal where no aggregation was observed (GT platelets mixed with ADP or EPI) , of intermediate level where primary aggregation alone occurred (SPD platelets with all agents or with GT platelets with RI), and similar to normal where secondary aggregation was induced (B-S platelets stirred with ADP or EPI). The results suggest that the defective 3H-glycerol uptake by abnormal platelets is a consequence rather than a cause of the decrease in platelet aggregation. Enhanced PI turnover most probably reflects the cells response to membrane damage or distortion incurred during aggregation and the release reaction.

Incorporation of3H-Glycerol into Phospholipids of Normal and abnormal Platelets