Threshold of Microvascular Occlusion: Injury Size Defines the Thrombosis Scenario

被引:33
作者
Belyaev, Aleksey V. [1 ,2 ]
Panteleev, Mikhail A. [1 ,2 ,3 ,4 ]
Ataullakhanov, Fazly I. [1 ,2 ,3 ,4 ]
机构
[1] RAS, Ctr Theoret Problems Physicochem Pharmacol, Moscow 117901, Russia
[2] Fed Res & Clin Ctr Pediat Hematol Oncol & Immunol, Moscow, Russia
[3] Moscow MV Lomonosov State Univ, Dept Phys, Moscow, Russia
[4] HemaCore LLC, Moscow, Russia
基金
俄罗斯科学基金会;
关键词
BLOOD-FLOW-VELOCITY; PLATELET-ADHESION; TISSUE FACTOR; SHEAR RATE; IN-VIVO; INTRAVENOUS THROMBOLYSIS; COLLAGEN SURFACES; GROWTH-RATE; SUBENDOTHELIUM; FIBRIN;
D O I
10.1016/j.bpj.2015.06.019
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
Damage to the blood vessel triggers formation of a hemostatic plug, which is meant to prevent bleeding, yet the same phenomenon may result in a total blockade of a blood vessel by a thrombus, causing severe medical conditions. Here, we show that the physical interplay between platelet adhesion and hemodynamics in a microchannel manifests in a critical threshold behavior of a growing thrombus. Depending on the size of injury, two distinct dynamic pathways of thrombosis were found: the formation of a nonocclusive plug, if injury length does not exceed the critical value, and the total occlusion of the vessel by the thrombus otherwise. We develop a mathematical model that demonstrates that switching between these regimes occurs as a result of a saddle-node bifurcation. Our study reveals the mechanism of self-regulation of thrombosis in blood microvessels and explains experimentally observed distinctions between thrombi of different physical etiology. This also can be useful for the design of platelet-aggregation-inspired engineering solutions.
引用
收藏
页码:450 / 456
页数:7
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