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Effect of cardiac rehabilitation on endogenous nitric oxide production in cardiac patients

心脏康复对心脏病患者内源性一氧化氮生成的影响

基本信息

批准号：
13670690
负责人：
MATSUMOTO Akihiro
金额：
$ 2.3万
依托单位：
The University of Tokyo
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2002
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13670690/
关键词：
cardiac rehabilitation cardiac diseases nitric oxide brain natriuretic peptide atrial natriuretic peptide neuro-humoral factor anaerobic threshold peak oxygen uptake 心筋梗塞嫌気性代謝閾値慢性心不全

项目摘要

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.

在心肌梗死和充血性心力衰竭的心脏病患者中通常观察到内皮依赖性血管舒张减弱。最近，它已被证明，一氧化氮（NO），内皮衍生的舒张因子，在人体呼出的空气中检测。我们已经证明，运动可以急性增加正常对照组呼出空气中的NO输出，并且其增加在心脏疾病如心肌梗死和充血性心力衰竭中减弱。虽然它已被证明，慢性运动训练可以改善这种衰减的内皮依赖性血管舒张的前臂体积描记法的研究，目前还不清楚，运动训练可能会增加内源性NO的生产在休息和运动。我们测量了呼出NO输出（VNO）作为其在肺部的本地生产的指标，在有限的直立自行车运动之前和之后的运动训练心肌梗死和充血性心力衰竭的心脏病患者。运动训练提高了无氧阈、摄氧量和运动负荷。运动过程中NO浓度和VNO增加。运动训练可降低血浆BNP和ANP水平。这些结果表明，运动训练增加内源性NO的产生，并可能内皮依赖性血管舒张，导致改善心功能和运动不耐受。