2002 Fiscal Year Final Research Report Summary
Effect of cardiac rehabilitation on endogenous nitric oxide production in cardiac patients
| Project/Area Number |
13670690
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MATSUMOTO Akihiro The University of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (70323574)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAJIMA Toshiaki The University of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (50227790)
TAKENAKA Katsu The University of Tokyo, Faculty of Medicine, Lecturer, 医学部附属病院, 講師 (20188204)
HIRATA Yasunobu The University of Tokyo, Faculty of Medicine, Lecturer, 医学部附属病院, 講師 (70167609)
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| Project Period (FY) |
2001 – 2002
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| Keywords | cardiac rehabilitation / cardiac diseases / nitric oxide / brain natriuretic peptide / atrial natriuretic peptide / neuro-humoral factor / anaerobic threshold / peak oxygen uptake |
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| Research Abstract |
Attenuated endothelium-dependent vasodilatation is commonly observed in cardiac patients with myocardial infarction and congestive heart failure. Recently, it has been shown that nitric oxide (NO), an endothelium-derived relaxing factor, is detected in the exhaled air in humans. We have demonstrated that exercise can acutely increase NO output in the exhaled air in normal control subjects, and that its increase is attenuated in cardiac diseases such as myocardial infarction and congestive heart failure. Although it has been shown that chronic exercise training can improve this attenuated endothelium-dependent vasodilatation by the study of forearm plethysmography, it is unclear that exercise training may increase endogenous NO production at rest and during exercise. We measured exhaled NO output (VNO) as indicator of its local production in the lungs during symptom-limited upright bicycle exercise before and after exercise training in cardiac patients with myocardial infarction and congestive heart failure. Exercise training increased anaerobic threshold, oxygen uptake and work load at peak exercise. It also increased NO concentration and VNO during exercise. Exercise training decreased plasma BNP and ANP. These findings suggested that exercise training increased endogenous NO production, and probably endothelium-dependent vasodilatation, leading to improvement in cardiac function and exercise intolerance.
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