Why the study?
Does short-acting high shear stress directly induce platelet activation?
Does short-acting high shear stress directly induce platelet activation?
Direct shear-induced platelet activation is unlikely and appears mostly secondary to biochemical activation by mediators from passively destroyed platelets.
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Short high-shear stress does not directly activate platelets; leaves open confirmation in human in vivo models.
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 beta-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 reducible 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.
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Wurzinger et al. (1985) studied this question.
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