scholarly journals Microarterial anastomoses: A parameterised computational study examining the effect of suture position on intravascular blood flow

2016 ◽  
Vol 105 ◽  
pp. 141-148 ◽  
Author(s):  
R.A.J. Wain ◽  
D. Hammond ◽  
M. McPhillips ◽  
J.P.M. Whitty ◽  
W. Ahmed
Author(s):  
Shigefumi Tokuda ◽  
Takeshi Unemura ◽  
Marie Oshima

Cerebrovascular disorder such as subarachnoid hemorrhage (SAH) is 3rd position of the cause of death in Japan [1]. Its initiation and growth are reported to depend on hemodynamic factors, particularly on wall shear stress or blood pressure induced by blood flow. In order to investigate the information on the hemodynamic quantities in the cerebral vascular system, the authors have been developing a computational tool using patient-specific modeling and numerical simulation [2]. In order to achieve an in vivo simulation of living organisms, it is important to apply appropriate physiological conditions such as physical properties, models, and boundary conditions. Generally, the numerical simulation using a patient-specific model is conducted for a localized region near the research target. Although the analysis region is only a part of the circulatory system, the simulation has to include the effects from the entire circulatory system. Many studies have carried out to derive the boundary conditions to model in vivo environment [3–5]. However, it is not easy to obtain the biological data of cerebral arteries due to head capsule.


2015 ◽  
Vol 3 (1) ◽  
pp. 27-34 ◽  
Author(s):  
Hamidreza Ghasemi Bahraseman ◽  
Bahareh Hamzehei ◽  
Karim Leilnahari ◽  
Arezoo Khosravi ◽  
Ehsan Mohseni Languri

1998 ◽  
Vol 18 (9) ◽  
pp. 998-1007 ◽  
Author(s):  
Kenneth Revett ◽  
Eytan Ruppin ◽  
Sharon Goodall ◽  
James A. Reggia

When a cerebral infarction occurs, surrounding the core of dying tissue there usually is an ischemic penumbra of nonfunctional but still viable tissue. One current but controversial hypothesis is that this penumbra tissue often eventually dies because of the metabolic stress imposed by multiple cortical spreading depression (CSD) waves, that is, by ischemic depolarizations. We describe here a computational model of CSD developed to study the implications of this hypothesis. After simulated infarction, the model displays the linear relation between final infarct size and the number of CSD waves traversing the penumbra that has been reported experimentally, although damage with each individual wave progresses nonlinearly with time. It successfully reproduces the experimental dependency of final infarct size on midpenumbra cerebral blood flow and potassium reuptake rates, and predicts a critical penumbra blood flow rate beyond which damage does not occur. The model reproduces the dependency of CSD wave propagation on N-methyl-D-aspartate activation. It also makes testable predictions about the number, velocity, and duration of ischemic CSD waves and predicts a positive correlation between the duration of elevated potassium in the infarct core and the number of CSD waves. These findings support the hypothesis that CSD waves play an important causal role in the death of ischemic penumbra tissue.


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