Project/Area Number |
16K10933
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Anesthesiology
|
Research Institution | Mie University |
Principal Investigator |
Zhang Erquan 三重大学, 医学系研究科, 助教 (30456727)
|
Co-Investigator(Kenkyū-buntansha) |
丸山 一男 三重大学, 医学系研究科, 教授 (20181828)
澤田 博文 三重大学, 医学系研究科, 講師 (30362354)
丸山 淳子 鈴鹿医療科学大学, 医用工学部, 教授 (50263017)
|
Project Period (FY) |
2016-04-01 – 2019-03-31
|
Project Status |
Completed (Fiscal Year 2018)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | pulmonary hypertension / 肺高血圧症 / 組織 / 生理学 |
Outline of Final Research Achievements |
Treatment of pulmonary arterial hypertension is difficult.The major causes of PAH are right heart failure caused by congenital heart disease with left-right shunt, ARDS, neonatal persistent pulmonary hypertension, collagen disease, pulmonary fibrosis, idiopathic pulmonary arterial hypertension, etc. Inhibitory effects of KNO3 was investigated in pulmonary arteries of chronic hypoxia-induced hypertension rats. Mean pulmonary arterial pressure and right ventricular hypertrophy were significantly increased by hypoxic exposure, resulting in hypoxic-induced pulmonary hypertension model. Results such as mean pulmonary arterial pressure (mPA), mean pulmonary arterial pressure / mean arterial blood pressure (mPA / mAP), and right ventricular hypertrophy (RVH) were significantly increased by chronic hypoxia-induced hypertension, but inhibition of KNO3 was not observed.Suppressive effect of KNO3 that were not obtained on chronic hypoxia-induced pulmonary hypertension should be further examined.
|
Academic Significance and Societal Importance of the Research Achievements |
本課題の学術的意義では、硝酸イオン・亜硝酸イオンを摂取するとNOSに依存しない、NO生成が高まることが期待できる。硝酸―亜硝酸―NO系による、肺高血圧発症抑制効果を調べるため、実験的肺高血圧ラットに硝酸イオン水・亜硝酸イオン水を経口投与し、①硝酸、亜硝酸の体内動態とNO生成(リサイクルされたNO)を調べ、②肺高血圧と肺動脈血管病変の発生・進展に対する抑制効果を明らかにし、③血管内膜の細胞性・線維性増殖への影響を調べる。社会的意義は、亜硝酸イオン(KNO3)の慢性低酸素肺高血圧症に対する抑制効果があれば、肺高血圧症に対する新し治療法ができ、コストも安くなる。
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