2000 Fiscal Year Final Research Report Summary
Investigation of the mechanism in localization of atherosclerosis by computational analysis of mass transfer from flowing blood to an arterial wall based on a true-to-scale anatomical model
| Project/Area Number |
11680831
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biomedical engineering/Biological material science
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
WADA Shigeo Hokkaido Univ., Research Institute for Electronic Science, Lecturer, 電子科学研究所, 講師 (70240546)
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| Project Period (FY) |
1999 – 2000
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| Keywords | Computational biomechanics / Blood flow / Mass transfer / Atherosclerosis / Intimal hyperplasia / lipoprotein / Hemodynamics |
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| Research Abstract |
To elucidate the mechanism in the localization of vascular diseases such as atherosclerosis and anastomotic intimal hyperplasia in the arterial system, we carried out computational analyses of mass transport of atherogenic low density lipoproteins (LDL) from flowing blood to an arterial wall based on true-to-scale anatomical models which were obtained by animal experiments creating a mild stenosis on rabbit common carotid arteries and an end-to-side anastomotic junction on dog common carotid arteries and harvesting them at different time postoperatively. To do that, we developed an experimental system measuring the 3-dimensional configuration of a resinous cast of real artery and a new modeling method to construct anatomically a realistic model for computation from the configuration of the arterial cast. We also measured the location where intimal hyperplasia occurred and the distribution of intimal thickness in the arteries which were used to construct the computational model by microscopic observation of histological specimens prepared from the arteries. Then the relationship among the hemodynamic properties such as wall shear stress and detailed flow patterns in the vicinity of the vessel wall, LDL concentration at the luminal surface of the vessel and the thickness of the intima was investigated. As the result, it was found that LDL concentration at the luminal surface of the artery was locally elevated distal to the apex of the stenosis and at heel and toe portions of the anastomotic junction where flow was disturbed and wall shear stress was relatively low, and that such a site corresponded well to the site where intimal thickening was observed. These results suggest that blood flow plays an important role in the localized pathogenesis and development of atherosclerosis and intimal hyperplasia by affecting the degree of concentration polarization of LDL which occurs at a blood/endothelium boundary.
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