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For flowing blood, the semisolid RBCs collide and rotate at a rate that depends on local shear rates and the local concentration of particles (18–23).

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Lastly, thrombus embolization and removal may occur (37).

This process has been observed experimentally, but little data exist as to the incidence or rate of this process. Atherosclerosis produces a lesion that narrows the arterial lumen over time, creating a stenosis.

Thrombus formation over a ruptured atherosclerotic plaque cap can occlude an artery with fatal consequences.

We describe a computational model of platelet transport and binding to interpret rate-limiting steps seen in experimental thrombus formation over a collagen-coated stenosis.

Arterial thrombosis leads to the vast majority of acute myocardial infarction and stroke cases (1–4).

Recent studies have identified the importance of high shear rates on platelet adhesion and aggregation (5–17).

High shear rates exist near the stenosis apex, which is where rapid platelet accumulation can occur (5–11).

The hemodynamics around a stenosis are pathophysiological with large changes in shear rate and the potential for flow separation, providing a rich, complex environment in which to compare a model with experimental thrombus growth.

We have previously reported on the experimental creation of thrombus under high shear, near a stenosis, that grows to full occlusion and is consistent with clinical disease (11,38,39).

These thrombi grow very rapidly and are platelet-rich, with platelets comprised of ~80% of the thrombus.

It is possible that the transport of platelets confers the shear rate dependence separately from the binding, which may or may not be shear stress-dependent.

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