| Project/Area Number |
16390458
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
KINOSHITA Hiroyuki Wakayama Medical University, School of Medicine, Associate Professor, 医学部, 助教授 (70291490)
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| Co-Investigator(Kenkyū-buntansha) |
HATANO Yoshio Wakayama Medical University, School of Medicine, Professor, 医学部, 教授 (70115913)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 2006: ¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2005: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2004: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Spinal microarterioles / Nitric oxide / Synthase / Gene knockout mice / Carbon dioxide / 脊髄内動脈 / カリウムチャネル |
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| Research Abstract |
Spinal slices (150 μm thick) were prepared from the rat or mouse spinal cords. Slices were continuously superfused with control solution at the flow rate of 1.5 ml/min, bubbled with 93% O_2 + 7% CO_2 (PCO_2 = 40 mmHg, pH = 7.4, 37℃). An intraparenchymal arteriole (5.0-10.0 μm in internal diameter) was located within the neuronal tissue, and its internal diameter was continuously monitored with the live computerized videomicroscopy. The videomicroscopy equipment consisted of an inverted microscope. The image of a parenchymal arteriole was transmitted to video camera (C6790-81, Olympus, Tokyo, Japan) and displayed on a computer via a media converter (Physio-Tech, Tokyo, Japan). Changes of intraluminal diameter in spinal microvessels were recorded on computer image files and then analyzed using the image software.
During contraction to prostaglandin F_<2α> (0.5 μM), hypercapnia (PCO_2 = 50 mmHg produced by 10% CO2) induced dilation of intraparenchymal spinal arterioles. Addition of acetylcholine (0.1 μM) also induced dilation of these arterioles in the spinal slice from normal mice, whereas this concentration of acetylcholine did not induce dilation of arterioles in the slice from neuronal nitric oxide synthase knockout mice. Effects of anesthetics on above vasodilator responses are under investigation.
These results suggest that in spinal microarterioles, carbon dioxide play a role as a vasodilator substance and that neuronal nitric oxide synthase contributes to spinal vasodilator responses induced by physiological agents including acetylcholine.
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