| Project/Area Number |
08671627
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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 |
Cerebral neurosurgery
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| Research Institution | National Cardiovascular Center Research Institute |
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Principal Investigator |
SEKI Junji Natl Cardiovasc Ctr Res Inst, Dept Biomed Eng, Research Fellow, 生体工学部, 室長 (20163082)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAMIZAWA Keiichi Natl Cardiovasc Ctr Res Inst, Dept Biomed Eng, Research Fellow, 生体工学部, 室員 (10163312)
MATSUDA Takehisa Natl Cardiovasc Ctr Res Inst, Dept Biomed Eng, Head of Dept, 生体工学部, 部長 (60142189)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Brain Pial Microvessels / Laser-Doppler Anemometer / Amplitude of Pulsation / Intravascular Pressure / Nitric Oxide / Wall Shear Stress / Vessel Wall Elasticity / Intracranial Pressure / Transmural Pressure / モデル解析 |
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| Research Abstract |
This research projecto was aimed to analyze the blood flow dynamics undr the various pathological conditions using our developed fiber-optic laser-Doppler anemometer microscope (FLDAM). In particular, effects of incresed intracranial pressure on the pulse wave propagation along the pial arteriolar network and effects of nitric oxide on the velocity distributions in the pial microvessels were studied.
To observe the brain pial microcirculation, a closed cranial window was created on the parietal region of the rats. The red cell velocity in single pial microvessels was measured by the FLDAM.The internal pressure of the window, which is equal to the intracranial pressure, was changed between 0 and 50 mmHg. The red cell velocity in arterioles showed regular pulsatile waveforms synchronous with the systemic arterial pressure measured in the femoral artery. The amplitude of velocity pulsation was defined as the half of the difference between the maximum and minimum of the ensemble average vel
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ocity using the systemic pressure as a timing signal. The amplitude of velocity pulsation in the pial arterioles was 24 (]SY.+-。[) 9%, 29 (]SY.+-。[) 9% and 40 (]SY.+-。[) 11% at ICP = 5,30 and 50 mmHg, respectively. It increased gradually with ICP on the average. In individual arterioles, however, the amplitude of velocity pulsation showed a sharp increase at a certain critical value of ICP.The critical ICP ranged between 25 and 40 mmHg, increased with increasing vessel diameter and decreased from upstream to downstream along arteriolar trees. Theoretical calculations wereconducted based on a model assuming that the elastic modulus of arteriolar wall is a step function of transmural pressure and the network architecture is approximated by a porous tapered elastic tube. They suggest that the critical ICP corresponds to the internal pressure of the arteriole.
Constant shear stress hypothesis has been introduced to explain the cubic dependence of the volumetric flow in arterioles on vessel diameter. The mechanism of the hypothesis is based on the flow dependent vasodilation mediated by nitric oxide (NO). However, our measurements by the FLDAM revealed that the flow rate in the rat pial arterioles is proportional to the 3.46 (]SY.+-。[) 0.18<@D2-@>D2th power of the diameter, which is significantly different from 3. To investigate the effects of NO on the velocity distribution, the red cell velocity was measured in the pial arterioles with diameter between 20 and 60 mum under the infusion of sodium nitoprusside (SNP,a potent NO donor). Both diamete and mean velocity increased by 14% on the average. The distributions of mean velocity and wall shear rate did not show significant changes compared to the control condition. Less
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