Rheology of thrombotic processes in flow: The interaction of erythrocytes and thrombocytes subjected to high flow forces 1

Abnormally high shear stresses (T_w > 50–200 Pal are known to occur under exceptional conditions in vivo (e.g. during the formation of a hemostatic plug in a rapidly perfused artery after it has been cut). Likewise, blood flow over a stenosis and blood flow through many artificial organs produces shear stresses in the same order of magnitude.

Shear stresses above 50 Pa are known to damage red cells and platelets. It is hypothesized that such “damage” of the blood cells provides a physiological stimulus which triggers key events of platelet activation (directly and indirectly via release of ADP from ruptured red blood cells) and of the coagulation enzymes (via the demasking of procoagulatory phospholipids). Experiments are described in which the occurrence of the postulated biochemical events is documented under conditions of high shear tube flow.

The concept of shear activation of platelets is incorporated in a combined biochemical-hemorheological theory of high shear thrombotic events such as they occur in arteries. In this theory, the process of thrombosis in high flow is considered to be initiated (on the afferent limb) by abnormally high shear stresses, but manifests itself subsequent to autokatalytic augmentation as the formation of white thrombi and deposits onto a wall (efferent limb).