Physiological functions of the endothelial cells in relation to the to the mass transport at carotid bifurcation
| Project/Area Number |
16560137
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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 |
Fluid engineering
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| Research Institution | Tokyo Institute of Technology |
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Principal Investigator |
TADA Shigeru Tokyo Institute of Technology, Mechanical Engineering, Assistant Professor, 大学院理工学研究科, 助手 (70251650)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2004: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Endothelial cells / Wall shear stress / Mass transport / Oxygen / Nitric Oxide / Fluorescent microscope imaging / Carotid bifurcation / Atherosclerosis / 一酸化炭素 / 勁動脈分岐部 / 低酸素症 / シグナル伝達 |
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| Research Abstract |
The purpose of the present research project was to investigate physiological functions of vascular endothelial cells in relation to the mechanism of mass transport at the carotid bifurcation.
Firstly, we studied oxygen mass transfer in the human carotid bifurcation, focusing on the effects of the wall compliance and flow field on the temporal variation and spatial distribution of the oxygen wall flux. Details of unsteady convective-diffusive oxygen transport were examined numerically using a compliant model of the human carotid bifurcation and realistic blood flow waveforms. Results reveal that axial flow separation at the outer common-internal carotid wall can significantly alter the flow field, oxygen tension field, and oxygen wall flux distribution. At the outer wall of the sinus, the Sherwood number, Sh (non-dimensional oxygen wall flux), takes on significantly lower values than at other sites due to the attenuation of transport rates by convective flow away from wall. More specifically, the lowest value of Sh was Sh〜6 (in the sinus), which is much lower than the value of the non- dimensional oxygen consumption rate (Damkohler number, Da) in the reactive wall tissue (Da=29-39).
Next, in order to address the role of nitric oxide and its downstream mechanism in the localization of atherosclerosis, the effects of mass transport and hemodynamics on endothelial cells functions were investigated. An in vitro experiment model that simulates in vivo spatial patterns of flow separation, recirculation, and reattachment have been developed to examine the release of nitric oxide (NO) from the endothelial cell layer in response to the shear stress with a complex spatial variation. Direct exposure of cells to 20dyne/cm2 shear stress after the onset of flow induced a rapid elevation in the nitric oxide release in the first ten minutes followed by a less rapid production.
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Report
(3 results)
Research Products
(13 results)
