Dysregulation of endogenous carbon monoxide and nitric oxide production in patients with advanced ischemic or nonischemic cardiomyopathy.
Dysregulation of endogenous carbon monoxide and nitric oxide production in patients with advanced ischemic or nonischemic cardiomyopathy.
复制标题
晚期缺血性或非缺血性心肌病患者内源性一氧化碳和一氧化氮生成失调。
DOI：
10.1016/s0002-9149(03)00890-7
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发表时间：
2003
期刊：
影响因子：
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通讯作者：
Migrino,RaymondQ
中科院分区：
文献类型：
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作者：
Seshadri,Niranjan;Dweik,RaedA;Laskowski,Daniel;Pothier,Claire;Rodriguez,Leonardo;Young,JamesB;Migrino,RaymondQ
一氧化碳（CO）和一氧化氮（NO）是内源性血管调节分子，其在心力衰竭中的作用尚不完全清楚。呼出CO和NO的测量提供了新的非侵入性评估其内源性生产。我们比较了24例晚期缺血性和非缺血性心肌病患者和13例无已知心脏病的对照组在静息时和运动试验后1分钟和5分钟时呼出的CO和NO。心肌病患者静息时呼出的CO较低（1.66 ± 0.2 vs 1.80 ± 0.5 ppm，p = 0.02）和运动后1分钟（1.35 ± 0.2 vs 1.81 ± 0.5 ppm，p = 0.009），运动后5分钟的趋势相似（1.45 ± 0.3 vs 1.81 ± 0.5 ppm，p = 0.14）。心肌病患者运动后呼出的CO减少（静息时与运动后1分钟和5分钟分别为p <0.001和p = 0.02），但对照组保持不变。心肌病患者和对照组在静息时（9.48 ± 1.4 vs 9.68 ± 1.5 ppb，p = NS）和运动后（1分钟：10.91 ± 1.8 vs 9.19 ± 1.2 ppb; 5分钟：10.52 ± 1.5 vs 8.90 ± 1.2 ppb，p = NS）的呼出NO无差异。心肌病患者运动后呼出的NO增加（分别为p = 0.01和p = 0.04休息与运动1分钟和5分钟），但在对照组中保持不变。心肌病患者呼出CO、NO与峰值耗氧量无相关性。心肌病患者和正常对照者在休息或运动时呼出的CO和NO的不同反应可能指向内源性CO和NO产生的失调。
Carbon monoxide (CO) and nitric oxide (NO) are endogenous vasoregulatory molecules whose role in heart failure is not fully known. Exhaled CO and NO measurement provide novel noninvasive assessment of their endogenous production. We compared exhaled CO and NO in 24 patients with advanced ischemic and nonischemic cardiomyopathy and in 13 control subjects without known cardiac disease at rest and at 1 and 5 minutes after exercise testing. Exhaled CO was lower in patients with cardiomyopathy at rest (1.66 ± 0.2 vs 1.80 ± 0.5 ppm, p = 0.02) and 1 minute after exercise (1.35 ± 0.2 vs 1.81 ± 0.5 ppm, p = 0.009), with a similar trend at 5 minutes after exercise (1.45 ± 0.3 vs 1.81 ± 0.5 ppm, p = 0.14). Exhaled CO decreased in patients with cardiomyopathy after exercise (p <0.001 and p = 0.02 at rest vs 1 and 5 minutes after exercise, respectively) but was maintained in controls. Exhaled NO did not differ between patients with cardiomyopathy and controls at rest (9.48 ± 1.4 vs 9.68 ± 1.5 ppb, p = NS) and after exercise (1 minute: 10.91 ± 1.8 vs 9.19 ± 1.2 ppb; 5 minutes: 10.52 ± 1.5 vs 8.90 ± 1.2 ppb, p = NS). Exhaled NO increased after exercise in patients with cardiomyopathy (p = 0.01 and p = 0.04 rest vs exercise at 1 and 5 minutes, respectively), but was maintained in controls. Exhaled CO and NO were not correlated with peak oxygen consumption in patients with cardiomyopathy. The differential responses in exhaled CO and NO at rest or with exercise between patients with cardiomyopathy and normal controls may point to dysregulation in endogenous CO and NO production.