@techreport{oai:mie-u.repo.nii.ac.jp:00013846,
 author = {張, 尓泉 and Zhang, Erquan and 丸山, 一男 and Maruyama, Kazuo and 澤田, 博文 and Sawada, Hirohumi and 丸山, 淳子 and Maruyama, Junko},
 month = {Sep},
 note = {application/pdf, 左ー右シャントを伴う先天性心疾患、ARDS、新生児遷延性肺高血圧、膠原病、肺線維症、特発性肺動脈高血圧症などでは、肺動脈圧の上昇から右心不全を来たし、治療に難渋する。慢性低酸素暴露肺高血圧ラットに対して、KNO3を用いての肺動脈血管病変の抑制効果について調べた。平均肺動脈圧と右心室肥大は低酸素暴露では有意に上昇、低酸素暴露肺高血圧症モデルができた。平均肺動脈圧、平均肺動脈血圧/平均動脈血圧、右心室肥大など結果では、低酸素暴露により有意に上昇したが、KNO3の投与により抑制が認められなかった。KNO3は慢性低酸素暴露肺高血圧症に対して抑制効果が認められなかった、続いて検討する必要がある。, 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 hyperttrophy were significantly increased by hypoxic exposure, resulting in hypoxic-induced pulmonary hypertension model. Result such as mean pulmonary arterial pressure (mPA), mean pulmonary arterial pressure / mean artirial 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., 2016年度～2018年度科学研究費補助金(基盤研究(C))研究成果報告書, 16K10933},
 title = {実験的肺高血圧に対する亜硝酸依存性ＮＯ合成機構の賦活による治療},
 year = {2019}
}