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  • Modelling thrombogenesis  (1)
  • Polymer and Materials Science  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Annals of biomedical engineering 18 (1990), S. 685-709 
    ISSN: 1573-9686
    Keywords: Thrombosis ; Transport in flowing blood ; Coagulation cascade ; Modelling thrombogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine , Technology
    Notes: Abstract The paper presents a mathematical analysis of the contributions of flow and mass transport to a single reactive event at a blood vessel wall. The intent is to prepare the ground for a comprehensive study of the intertwining of these contributions with the reaction network of the coagulation cascade. We show that in all vessels with local mural activity, or in “large” vessels (d〉0.1 mm) with global reactivity, events at the tubular wall can be rigorously described by algebraic equations under steady conditions, or by ordinary differential forms (ODEs) during transient conditions. this opens up important ways for analyzing the combined roles of flow, transport, and coagulation reactions in thrombosis, a task hitherto considered to be completely intractable. We report extensively on the dependence of transport coefficient kL and mural coagulant concentration Cw on flow, vessel geometry, and reaction kinetics. It is shown that for protein transport, kL varies only weakly with shear rate $$\dot \gamma $$ in large vessels, and not at all in the smaller tubes (d〈10−2 mm). For a typical protein, kL∼10−3 cm s−1 within a factor of 3 in most geometries, irrespective of the mural reaction kinetics. Significant reductions in kL (1/10–1/1,000) leading to high-coagulant accumulation are seen mainly in stagnant zones vicinal to abrupt expansions and in small elliptical tubules. This is in accord with known physical observations. More unexpected are the dramatic increases in accumulation which can come about through the intervention of an autocatalytic reaction step, with Cw rising sharply toward infinity as the ratio of reaction to transport coefficient approaches unity. Such self-catalyzed reactions have the ability to act as powerful amplifiers of an otherwise modest influence of flow and transport on coagulant concentration. The paper considers as well the effect on mass transport of transient conditions occasioned by coagulation initiation or pulsatile flow. During initiation, instantaneous flux varies with diffusivity and bulk concentration, favouring the early adsorption/consumption of proteins with the highest abundance and mobility. This is akin to the ‘Vroman effect’ seen in narrow, stagnant spaces. The effect of flow pulsatility on kL has the potential, after prolonged cycling, of bringing about segregation or accumulation of proteins, with consequences for the coagulation process.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Hoboken, NJ : Wiley-Blackwell
    Journal of Biomedical Materials Research 23 (1989), S. 1315-1326 
    ISSN: 0021-9304
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine , Technology
    Notes: The present article builds on elementary fluid dynamics and previous analyses by the author to delineate approximate boundaries of mural thrombus height HP, maximum shear rate \documentclass{article}\pagestyle{empty}\begin{document}$ \dot \gamma _{{\rm Max}} $\end{document}, and flow pulsatility beyond which thrombi are subject to either very high or very low probabilities of embolization. A thrombus height of ∼0.1 mm emerges as a critical dividing line: Below it, the maximum embolizing shear stress τs is independent of thrombus height and varies only linearly with shear rate. Above it, τs quickly approaches a strong quadratic dependence on both thrombus height and shear rate: \documentclass{article}\pagestyle{empty}\begin{document}$ \tau _{\rm s} \sim (H_{\rm p} \dot \gamma)^2 $\end{document}, significantly increasing the likelihood of an embolizing event. By contrast, convective-diffusive removal of blood components during the initial stages of thrombus formation varies only weakly with \documentclass{article}\pagestyle{empty}\begin{document}$ \dot \gamma ^{{1 \mathord{\left/ {\vphantom {1 3}} \right. \kern-\nulldelimiterspace} 3}} $\end{document} in all but the smallest vessels. These maximum embolizing stresses are due principally to fluid drag. Acceleration (pulsatile) forces only begin to make their presence felt at \documentclass{article}\pagestyle{empty}\begin{document}$ {\dot \gamma} $\end{document} 〈 500 s-1 and reach parity with fluid drag at \documentclass{article}\pagestyle{empty}\begin{document}$ {\dot \gamma} $\end{document} ∼ 10 s-1, i.e., at a level where the presence of pulsatility is questionable. The results are used to provide maps of domains with high and low probabilities of an embolytic event and of vessel patency. The maps reveal that relatively modest changes in shear rate and/or vessel lumen can cause shifts from high to low likelihood of vessel patency, opening up possible ways of controlling blockage by manipulation of these variables.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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