Elucidation of the transition mechanism of right ventricular hypertrophy to failure due to chronic hypoxia

2015 Fiscal Year Final Research Report

• Project/Area Number: 25860184
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Environmental physiology(including physical medicine and nutritional physiology)
• Research Institution: National Cardiovascular Center Research Institute
• Principal Investigator: Inagaki Tadakatsu 国立研究開発法人国立循環器病研究センター, 研究所, 上級研究員 (20638366)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 右心肥大 / 右心不全 / 肺高血圧症 / 冠動脈 / 低酸素

Outline of Final Research Achievements

Pulmonary hypertension (PH) causes cardiac hypertrophy in right ventricles (RV), and eventually leads to RV failure due to persistently elevated ventricular afterload. We hypothesized that the mechanical stress of RV associated with increased afterload impairs vasodilative function of the right coronary artery (RCA) in PH. Using microangiography, we compared the vascular function of RCA in the PH and control rats. Endothelium-dependent and -independent vasodilative responses were significantly attenuated in the middle and small arteries in the severe PH rats and the presence of abnormal constriction mechanism was revealed in the right coronary circulation of severe PH rat. The observed impaired vasodilative function of RCA in PH model suggests that impaired RCA function might have causal relationship with RV failure in the patients with severe PH.

Free Research Field

循環生理学、運動生理学