Abstract
The relative contributions of physiologic activators and shear rates (G) on the formation and stability of platelet aggregates arising from platelets treated with widely clinically used nonsteroidal anti-inflammatory drugs such as acetylsalicylic acid (ASA) need to be characterized for conditions of low G believed to be important in vivo. In Part I of these studies it was found that platelets in human citrated platelet-rich plasma (PRP) undergo ADP-induced aggregation in laminar flow by apparently two distinct processes: a low ADP-dependent process, generating large visible aggregates stable only at low shear rates, and a higher ADP-threshold-dependent process yielding more complete and shear-resistant large aggregate formation. Similar studies of both macroaggregation (TA) and actual % aggregation (%PA) were made with ADP injections into PRP in the cone-in-plate device as a function of G and pre-treatments with ASA (200 μM) and indomethacin (10 μM). These drugs reduced %PA in part and yielded only reversible macro-aggregation for studies conducted at the higher [ADP] (4–6 μM) and at high G (≳ 120–150 sec −1), with no significant effects at low G (≲ 30 sec −1). The results are discussed in terms of a platelet stickiness factor ‘s’, ascribed to changes in fibrinogen binding sites reported for these drug actions, and related to in vivo flow and variable platelet activation conditions.
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