Platelet and coagulation parameters following millisecond exposure to laminar shear stress.

Blood flowing through artificial organs or arterial stenoses is subjected to high shear for short times. To clarify the effects of short acting high shear forces upon platelets, heparinized PRP was exposed to viscometric flow (57-255 N/m2; 7-700 ms). Before and after shear exposure beta-TG release, LDH liberation, platelet count, and ADP-induced aggregation were assayed. Stypven time-monitored platelet procoagulant activity, determined after heparin neutralization by protamine, proved to be the most sensitive indicator for shear-induced platelet alteration. A shear stress of 170 N/m2, acting for as short a time as 7 ms made available procoagulant phospholipids, whereas beta-TG and LDH liberation required 255 N/m2 for 7 ms, and ADP refractoriness was found only after 113 ms exposure to 255 N/m2. Under these conditions the percent release of beta-TG does not exceed the liberation of LDH, suggesting that the evidence for "shear induced platelet activation" from experiments with exposure times of minutes, is most likely a conventional biochemical rather than biophysical effect.

Towards a concept of thrombosis in accelerated flow: rheology, fluid dynamics, and biochemistry.

The predilection sites of arterial thrombosis are characterized by local increase in wall shear stress, flow separation with eddy formation and stagnation point flow. The defenders of high shear, as well as those of low shear theory of thrombogenesis, point to correlations of predilection sites and the respective flow abnormalities. Experimental evidence is provided, that high shear rates can damage both red cells and platelets, that lysed red cells constitute a potent platelet stimulant, due to their content of adenine nucleotides, and that platelets do not adhere to surfaces unless transported onto them by convective motion, the effectiveness of the platelet-wall interaction being enhanced by platelet activation. Based on these facts, a resolution of the contrast between high and low shear theory of thrombosis is attempted in a way, that the different flow regimens, with blood cells sequentially passing them, are each considered important and interdependent steps on the way to thrombosis.

Model experiments on platelet adhesion in stagnation point flow.

Experiments with glass models of arterial branchings and bends, perfused with bovine platelet rich plasma (PRP), revealed platelet deposition being strongly dependent on fluid dynamic factors. Predilection sites of platelet deposits are characterized by flow vectors directed against the wall, so-called stagnation point flow. Thus collision of suspended particles with the wall, an absolute prerequisite for adhesion of platelets to surfaces even as thrombogenic as glass, appears mediated by convective forces. The extent of platelet deposition is correlated to the magnitude of flow components normal to the surface as well as to the state of biological activation of the platelets. The latter could be effective by an increase in hydrodynamically effective volume, invariably associated with the platelet shape change reaction to biochemical stimulants like ADP. The effect of altered rheological properties of platelets upon their deposition and of mechanical properties of surfaces was examined in a stagnation point flow chamber. Roughnesses in the order of 5 microns, probably by creating local flow disturbances, significantly enhance platelet adhesion, as compared to a smooth surface of identical chemical composition.