Abstract:
:Platelet activation under blood flow is thought to be critically dependent on the autologous secretion of soluble platelet agonists (chemical activators) such as ADP and thromboxane. However, recent evidence challenging this model suggests that platelet activation can occur independent of soluble agonist signalling, in response to the mechanical effects of micro-scale shear gradients. A key experimental tool utilized to define the effect of shear gradients on platelet aggregation is the murine intravital microscopy model of platelet thrombosis under conditions of acute controlled arteriolar stenosis. This paper presents a computational structural and hydrodynamic simulation of acute stenotic blood flow in the small bowel mesenteric vessels of mice. Using a homogeneous fluid at low Reynolds number (0.45) we investigated the relationship between the local hydrodynamic strain-rates and the severity of arteriolar stensosis. We conclude that the critical rates of blood flow acceleration and deceleration at sites of artificially induced stenosis (vessel side-wall compression or ligation) are a function of tissue elasticity. By implementing a structural simulation of arteriolar side wall compression, we present a mechanistic model that provides accurate simulations of stenosis in vivo and allows for predictions of the effects on local haemodynamics in the murine small bowel mesenteric thrombosis model.
journal_name
J Biomechjournal_title
Journal of biomechanicsauthors
Tovar-Lopez FJ,Rosengarten G,Khoshmanesh K,Westein E,Jackson SP,Nesbitt WS,Mitchell Adoi
10.1016/j.jbiomech.2011.02.006subject
Has Abstractpub_date
2011-04-07 00:00:00pages
1031-9issue
6eissn
0021-9290issn
1873-2380pii
S0021-9290(11)00087-Xjournal_volume
44pub_type
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