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2019 Fiscal Year Final Research Report

Functions of Nitric Oxide and Endothelium-derived Hyperpolarizing Factor are impaired in Poor Run-off Autogenous Rabbit Arterial Grafts

Research Project

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Project/Area Number 17H04290
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Cardiovascular surgery
Research InstitutionNagoya University

Principal Investigator

KOMORI Kimihiro  名古屋大学, 医学系研究科, 教授 (40225587)

Co-Investigator(Kenkyū-buntansha) 杉本 昌之  名古屋大学, 医学部附属病院, 病院講師 (00447814)
伊藤 猛雄  名古屋市立大学, 医薬学総合研究院(医学), 研究員 (70159888)
坂野 比呂志  名古屋大学, 医学部附属病院, 講師 (80584721)
室原 豊明  名古屋大学, 医学系研究科, 教授 (90299503)
児玉 章朗  名古屋大学, 医学部附属病院, 病院講師 (10528748)
Project Period (FY) 2017-04-01 – 2020-03-31
Keywords内膜肥厚 / EDHF / 異常血流モデル / 内皮機能
Outline of Final Research Achievements

Background: Vascular endothelium induces smooth muscle cell (SMC) relaxation mainly mediated by endothelium-derived nitric oxide (EDNO) and endothelium-derived hyperpolarizing factor (EDHF). The present study was undertaken to determine whether the functions of EDNO and EDHF might be altered in poor run-off artery graft compared to “non-occluded graft”. Methods: The carotid artery was excised and implanted in its original position as an autogenous graft(“non-occluded graft”), and the most inferior branch of the external carotid artery served as the only outflow for the present conditions (“poor run-off graft”).
Conclusions: The functions of both EDNO and EDHF are impaired in poor run-off artery grafts.

Free Research Field

血管外科学

Academic Significance and Societal Importance of the Research Achievements

今回の結果より内皮由来過分極因子(EDHF)と血管内膜肥厚との関連が示唆され、EDHFをターゲットとした新しい治療戦略への発展が期待される。EDHFとグラフト内膜肥厚への関与、さらにはステント再狭窄との関連の研究は、閉塞性動脈硬化症だけではなく虚血性心血管病患者の晩期障害となる自家静脈、自家動脈グラフトの狭窄・閉塞、ステント再狭窄の病態解明を企図するもので、EDHFをターゲットとした新たな心血管病治療の可能性示唆し臨床的にも有用な結果であると思われた。

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Published: 2021-02-19  

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