| Project/Area Number |
25293295
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cardiovascular surgery
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| Research Institution | Nagoya University |
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Principal Investigator |
KOMORI Kimihiro 名古屋大学, 医学(系)研究科(研究院), 教授 (40225587)
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| Co-Investigator(Kenkyū-buntansha) |
BANNO HIROSHI 名古屋大学, 医学部附属病院, 講師 (80584721)
KODAMA AKIO 名古屋大学, 医学部附属病院, 講師 (10528748)
TABATA KOUKI 名古屋大学, 医学部附属病院, 医員 (20725832)
MUROHARA TOYOAKI 名古屋大学, 大学院医学系研究科, 教授 (90299503)
ITO TAKEO 名古屋市立大学, 大学院医学研究科, 教授 (70159888)
MAEKAWA TAKASHI 名古屋大学, 医学部附属病院, 助教 (70732684)
NARITA HIROSHI 名古屋大学, 医学部附属病院, 病院講師 (00528739)
SUGUMOTO MASAYUKI 名古屋大学, 医学部附属病院, 病院助教 (00447814)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥18,330,000 (Direct Cost: ¥14,100,000、Indirect Cost: ¥4,230,000)
Fiscal Year 2015: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥10,010,000 (Direct Cost: ¥7,700,000、Indirect Cost: ¥2,310,000)
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| Keywords | 血管内膜肥厚 / 自家動脈グラフト / EDHF |
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| Outline of Final Research Achievements |
The vascular endothelium induces smooth muscle relaxation mainly mediated by nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). The present study was undertaken to determine whether the functions of NO and EDHF may be altered in rabbit artery grafts.
At 28 days after the operation.Intimal hyperplasia was observed in "artery graft". When compared with "control artery","artery graft” exhibited greater acetylcholine-induced endothelium-dependent relaxation. Both the acetylcholine-induced increase in endothelial cell [Ca2+]i and the endothelium-dependent SMC hyperpolarization were weaker in "artery graft". Endothelial NO release under basal conditions was enhanced, while acetylcholine-induced endothelium-dependent SMC hyperpolarization was reduced in artery grafts.
It is suggested that enhanced NO production is responsible for the increased acetylcholine-induced endothelium-dependent relaxation, and for minimizing intimal hyperplasia, in a rabbit artery graft.
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