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Platelets were found to be stimulated by high shear exposure for 5 minutes. Using a new technique, shear stresses up to 255 N/m2, acting for pathophysiological relevant intervals of milliseconds did not elicit active release of β-TG, beyond the amount explained by LDH-monitored passive lysis. Neither the plasma level of ionized calcium (citrate vs heparin anticoagulation), nor a potent platelet inhibiting agent like PgI2(20 nM) did Significantly alter platelet responses to short acting high shear stress. Ultrastructural signs of activation could largely be suppressed by adding ADP-scavengers. Direct “shear induced platelet activation” appears rather unlikely and mostly reducable to secondary biochemical activation by mediators, probably adenine nucleotides, from a small percentage of passively shear-destroyed platelets. The extent of this secondary activation is largely a matter of experimental conditions.

A Couette viscometer with axial flow is proposed which allows blood to be exposed to defined shear stresses of short duration. A prototype of this viscometer is tested. By measurements and simple calculations the range of application is established. Measurements with blood show the possibility to control the flow conditions which may lead to haemolysis.