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

内皮依赖性血管舒张减弱常见于心肌梗死和充血性心力衰竭的心脏患者。最近，研究表明，一氧化氮（NO）是一种内皮来源的放松因子，在人体呼出的空气中被检测到。我们已经证明，运动可以急剧增加正常对照受试者呼出空气中的NO输出，并且在心肌梗死和充血性心力衰竭等心脏疾病中其增加减弱。尽管通过前臂体积描记研究表明，慢性运动训练可以改善这种减弱的内皮依赖性血管舒张，但尚不清楚运动训练是否可以增加休息和运动时的内源性NO生成。我们测量了伴有心肌梗死和充血性心力衰竭的心脏病患者在运动训练前后进行无症状的直立自行车运动时，呼出一氧化氮（VNO）作为其在肺部局部产生的指标。运动训练增加无氧阈值、摄氧量和运动高峰时的工作量。运动时一氧化氮浓度和VNO均升高。运动训练降低血浆BNP和ANP。这些发现表明，运动训练增加内源性NO的产生，并可能增加内皮依赖性血管舒张，从而改善心功能和运动不耐受。

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.