Platelet Function Following Surface Injury and Shear Stress: Adhesion, Aggregation, Release, and Factor 3 Activity*

Bernstein, Eugene F.; Marzec, Ulla M.; Clayman, Michael D.; Swanson, Sherri C.; Johnston, G. Gilbert

doi:10.1111/j.1749-6632.1977.tb41762.x

Cited by 17 publications

(5 citation statements)

References 26 publications

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“…This was indicated in jet-shearing tests reported by Bernstein et al 42 Given the probable viscoplastic nature of the platelet membrane and cytoplasm, this kind of inverse relationship between shear-induced lysis and duration of shear is to be expected.…”

Section: Plateletsmentioning

confidence: 75%

Flow-induced trauma to blood cells.

Sutera¹

1977

Circulation Research

129

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Section: Plateletsmentioning

confidence: 75%

Flow-induced trauma to blood cells.

Sutera¹

1977

Circulation Research

129

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“…Similar practices unifying the two shear stress measures with no distinction have also been adopted in studies focusing on shear-induced platelet damage. For example, Bernstein et al 2 used an apparatus similar to that one used by Forstrom 11 to generate a shear flow field and monitored the shearinduced platelet damage. A shear stress threshold for platelet damage is reported at the level of 10 5 N/m 2 in terms of the Reynolds shear stress.…”

Section: Introductionmentioning

confidence: 99%

“…Over the years a great deal of efforts has been dedicated to understanding the pathway from the BMHV induced hemodynamic stresses to blood cell damage. These efforts can be loosely categorized into studies aimed at: (1) understanding blood cell damage under controlled mechanical force environment; and (2) investigating the details of the mechanical environment induced by BMHV.…”

Section: Introductionmentioning

confidence: 99%

Characterization of Hemodynamic Forces Induced by Mechanical Heart Valves: Reynolds vs. Viscous Stresses

et al. 2007

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Bileaflet mechanical heart valves (BMHV) are widely used to replace diseased heart valves. Implantation of BMHV, however, has been linked with major complications, which are generally considered to be caused by mechanically induced damage of blood cells resulting from the non-physiological hemodynamics environment induced by BMHV, including regions of recirculating flow and elevated Reynolds (turbulence) shear stress levels. In this article, we analyze the results of 2D high-resolution velocity measurements and full 3D numerical simulation for pulsatile flow through a BMHV mounted in a model axisymmetric aorta to investigate the mechanical environment experienced by blood elements under physiologic conditions. We show that the so-called Reynolds shear stresses neither directly contribute to the mechanical load on blood cells nor is a proper measurement of the mechanical load experienced by blood cells. We also show that the overall levels of the viscous stresses, which comprise the actual flow environment experienced by cells, are apparently too low to induce damage to red blood cells, but could potentially damage platelets. The maximum instantaneous viscous shear stress observed throughout a cardiac cycle is <15 N/m(2). Our analysis is restricted to the flow downstream of the valve leaflets and thus does not address other areas within the BMHV where potentially hemodynamically hazardous levels of viscous stresses could still occur (such as in the hinge gaps and leakage jets).

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“…In the fifties a similar correlation was shown for arteries by comparison of thrombus localization obtained via stereoscopic post mortem arteriograms with the flow field in three-dimensional models of such sites (8) rotational viscosimeter demonstrated a dependency of coagulation time as well as thrombus composition on the shear rate applied (9). Exten sive work on the deposition of platelets in regions of disturbed flow, e. g. flow recirculation in branching and stenosis, has also been pro vided by Goldsmith and Karino as well as other authors (10)(11)(12)(13). Fibrin clotting has been linked to platelet deposition via release of thrombogenic substances which also can be liberated from blood cells damaged by high shear present in vessel stenosis (13,14).…”

Section: Introductionmentioning

confidence: 84%

Occlusive Thrombus Formation on Indwelling Catheters: In Vitro Investigation and Computational Analysis

Friedrich

Reininger²

1995

Thromb Haemost

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SummaryTo determine the hydrodynamic parameters involved in thrombus formation on indwelling catheters, fibrin coagulation was investigated in an in vitro model and compared with the prevailing flow field. Computational analysis was used to simulate clot growth and identify the variables which determine its localization. The fibrin clot grew from the distal end of the catheter along the interface between the bulk stream and the annular vortex located immediately downstream of the catheter tip, finally filling the entire vortex. The calculations of flow parameters for three different growth stages showed that regions of clot formation always correlated with regions exhibiting the longest residence time. Fibrin clotting could be simulated by a mathematical model using residence time as the only variable parameter. Our results demonstrate that the residence time is the single most important flow factor for fibrin coagulation and thus probably for thrombus formation. When the residence time equals the clotting time for the fluid, thrombus formation is initiated. Conversely, it ceases when the area of long fluid residence times is replaced by a fibrin clot. Hence the fibrin clot represents a hydrodynamic optimization of the previously disturbed flow.

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Platelet Function Following Surface Injury and Shear Stress: Adhesion, Aggregation, Release, and Factor 3 Activity*

Cited by 17 publications

References 26 publications

Flow-induced trauma to blood cells.

Flow-induced trauma to blood cells.

Characterization of Hemodynamic Forces Induced by Mechanical Heart Valves: Reynolds vs. Viscous Stresses

Occlusive Thrombus Formation on Indwelling Catheters: In Vitro Investigation and Computational Analysis

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