Pure platelet phosphatidylserine (PS) and phosphatidylethanolamine (PE) are compared with brain cephalin (Ceph) in clotting-tests; (1) two-stage, using (a) stypven, (b) trypsin, (c) autoprothrombin-C; (2) PTT (partial thromboplastin time); (3) TGT (thromboplastin generation test); all showing "prothromboplastic" activity, except PE in the unmodified TGT. In validated bioassays (1a), log-log plots of end point clotting-times against phosphatide concentrations are rectilinear and parallel. End points related to equivalents of prothrombin-activated (EPA), or thrombin yield (ETY), make possible computation of reactivities in mixtures. Unlike brain PS ("antithromboplastic"), platelet P-lipids show no inhibitor but summate quantitatively with each other or with Ceph. Alterations in lipid reactivities include: (i) decrease during storage, (ii) increase in desoxycholate, (both assayable), (iii) anomalous ("oxidative") increase, in thromboplastic enzyme tests, invalidating bioassays. TGT’s (3) do not show (iii), but can quantitate certain reactivities. Besides suggesting the basis for a physiologic thromboplastic role of platelets, these methods offer means to explore biochemical bases of reactivities in identifiable lipids. These may be partly related to certain enzymes or intermediates in blood clotting reactions.

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© 1963 by American Society of Hematology, Inc.
1963
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