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The shear rate (G) dependence of aggregate formation and stability of platelets in human citrated platelet-rich plasma (PRP) in laminar flow was studied for G=0-150 sec-1, a range encountered in many flow conditions, by injecting adenosine diphosphate (ADP) into PRP within a cone-in-plate device at 37°C. Macroaggregation was assessed by visual observation and light transmission (%T), as routinely done in aggregometry, while actual percent aggregation (PA) was determined by microscopy of sub-samples from the decrease in single platelet concentration. Control PA ≲ 8% (n=8), independent of G. Low [ADP] ≃ 0.75-1.5 μM, causing reversible aggregation in the aggregometer, gave shape change, and stable visible thrombus formation with maximal PA μ 25% at low G ≲ 30 sec-1; the apparent extent of aggregation (Δ%T) passed through a maximum at G μ 30 sec-1, with aggregate disruption occurring at G &gt; 30 sec-1. For high ADP ≳ 5 μM, causing stable maximal aggregation in the aggregometer, the rate of aggregation increased continuously with G, with PA 90% and visible thrombi stable for G=15-150 sec-1. Aspirin (200 μM) (n=8) or indomethacin (10 μM) (n=2) - treated platelets activated with high ADP ≳ 5-7.5 μM, exhibited the same stable aggregation at low G (≲ 30 sec-1) as found for untreated platelets; higher G ≲ 30 sec-1 yielded only reversible aggregation as seen in the aggregometer, with PA only partially inhibited. It seems that (1) at high [ADP] (≳ 5 μM), increasing G normally increases the rate of platelet aggregation without causing deaggregation, and (2) for [ADP] up to - 7.5 μM, in the absence of endoperoxide synthetase activation, shear stresses (τ) of only ≃ 1-3 dynes cm-2 prevent the formation of stable large thrombi though still allowing appreciable PA; sufficiently high ADP (10 μM) overcomes these τ destabilizing effects.

Human Platelet Aggregation In Laminar Flow: Stimulus And Shear Rate Dependence, With Effects Of Acetylsalicylic Acid