Studies on the Mechanisms of Shear-Induced Platelet Activation

Hellums, J. D.; Peterson, Dolores M.; Stathopoulos, NA; Moake, Joel L.; Giorgio, T.D.

doi:10.1007/978-3-642-71787-1_8

Cited by 79 publications

(76 citation statements)

References 33 publications

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“…They further confirm previous results, obtained largely in non-circulating systems, in which exposure of platelets to shear conditions on the same order as those found in the vascular pathologies, e.g., stenosed coronary arteries, cause significant platelet activation, which is dependent on both shear stress and exposure time. 12 The predictive capability of the DPIV technique was demonstrated by its ability to predict the same trend in vitro PAS assay experiments conducted in the same stenosis model geometries. The PAS recirculation results were conducted over 30 min of repeated passages through the stenosis models, i.e., are of bulk properties, while the DPIV/CFD are of single passages only.…”

Section: Discussionmentioning

confidence: 99%

“…19 Platelet responses have been identified under controlled experimental conditions. 3,4,9 Hellums et al 12 compiled numerous experimental results to depict a locus of incipient shear related platelet activation on a shear stress-exposure time plane, which is commonly used as a standard for the platelet activation threshold. That activation-criterion has been established under constant bulk stress, e.g., cone-and-plate devices, in which the shear level was kept constant while measuring the time to reach activation and then using flow cytometers for quantifying the degree of platelet activation.…”

Section: Introductionmentioning

confidence: 99%

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DPIV Prediction of Flow Induced Platelet Activation—Comparison to Numerical Predictions

et al. 2007

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Abstract-Flow induced platelet activation (PA) can lead to platelet aggregation, deposition onto the blood vessel wall, and thrombus formation. PA was thoroughly studied under unidirectional flow conditions. However, in regions of complex flow, where the platelet is exposed to varying levels of shear stress for varying durations, the relationship between flow and PA is not well understood. Numerical models were developed for studying flow induced PA resulting from stress histories along Lagrangian trajectories in the flow field. However, experimental validation techniques such as Digital Particle Image Velocimetry (DPIV) were not extended to include such models. In this study, a general experimental tool for PA analysis by means of continuous DPIV was utilized and compared to numerical simulation in a model of coronary stenosis. A scaled up (5:1) 84% eccentric and axisymetric coronary stenosis model was used for analysis of shear stress and exposure time along particle trajectories. Flow induced PA was measured using the PA State (PAS) assay. An algorithm for computing the PA level in pertinent trajectories was developed as a tool for extracting information from DPIV measurements for predicting the flow induced thrombogenic potential. CFD, DPIV and PAS assay results agreed well in predicting the level of PA. In addition, the same trend predicted by the DPIV was measured in vitro using the Platelet Activity State (PAS) assay, namely, that the symmetric stenosis activated the platelets more as compared to the eccentric stenosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

DPIV Prediction of Flow Induced Platelet Activation—Comparison to Numerical Predictions

et al. 2007

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“…They also analyzed results of previous research, and showed that the percentage of platelet trauma as a function of the product of bulk shear rate and residence time follows an exponential growth curve. Phenomenological studies of platelet response (11,12) led to a depiction of a locus of incipient shear-related platelet serotonin release on a shear stress-exposure time plane. Sutera et al (22) showed that pulsed exposure resulted in more platelet aggregation than continuous exposure for the same total exposure time to stress, indicating shear and velocity gradients as enhancing platelet activation.…”

Section: Introductionmentioning

confidence: 99%

Fluid mechanics of arterial stenosis: Relationship to the development of mural thrombus

et al. 1997

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AbstFact--In this study, we analyzed blood flow through a model stenosis with Reynolds numbers ranging from 300 to 3,600 using both experimental and numerical methods. The jet produced at the throat was turbulent, leading to an axisymmetric region of slowly recirculating flow. For higher Reynolds numbers, this region became more disturbed and its length was reduced. The numerical predictions were confirmed by digital particle image velocimetry and used to describe the fluid dynamics mechanisms relevant to prior measurements of platelet deposition in canine blood flow (R. T. Schoephoerster et al., Atheroscleros& and Thromboshr 12:1806-1813. Actual deposition onto the wall was dependent on the wall shear stress distribution along the stenosis, increasing in areas of flow recirculation and reattachment. Platelet activation potential was analyzed under laminar and turbulent flow conditions in terms of the cumulative effect of the varying shear and elongational stresses, and the duration platelets are exposed to them along individual platelet paths. The cumulative product of shear rate and exposure time along a platelet path reached a value of 500, half the value needed for platelet activation under constant shear (J. M. Ramstack et al., Journal of Biomechanics 12: 113-125, 1979).

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“…A critical value for accumulated shear stress above which platelets are considered activated is, for example, given by the Hellums activation threshold criterion, i.e. 3.5Ns/m 2 (Hellums et al, 1987;Dumont et al, 2007).…”

Section: Blood Damage and Bmhvsmentioning

confidence: 99%