Katz S D, Krum H, Khan T, Knecht M
Columbia Presbyterian Medical Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York, USA.
J Am Coll Cardiol. 1996 Sep;28(3):585-90. doi: 10.1016/0735-1097(96)00204-5.
This study was undertaken to investigate the role of endothelium-derived nitric oxide in the regulation of forearm blood flow during exercise in normal subjects and patients with congestive heart failure.
Nitric oxide-mediated vasodilation in response to muscarinic stimulation is impaired in the peripheral circulation of patients with congestive heart failure. Whether nitric oxide-mediated vasodilation during exercise is also impaired in patients with congestive heart failure is unknown.
Forearm blood flows (ml/min per 100 ml) were determined during rhythmic hand grip exercise at 15%, 30% and 45% of maximal voluntary contraction by venous occlusion plethysmography before and after regional inhibition of nitric oxide synthesis with administration of L-NG-monomethylarginine (L-NMMA) in the brachial artery of 17 patients with congestive heart failure (mean age 49 years, mean left ventricular ejection fraction 0.22) and 10 age-matched normal subjects.
Before administration of L-NMMA in the brachial artery, forearm blood flows in patients with congestive heart failure during rhythmic hand grip exercise at 15%, 30% and 45% of maximal voluntary contraction were slightly but not significantly lower than that of normal subjects ([mean +/- SE] 6.8 +/- 1.0, 8.5 +/- 1.0 and 12.9 +/- 1.7 ml/min per 100 ml, respectively, in patients with congestive heart failure vs. 6.6 +/- 1.2, 11.6 +/- 1.9 and 16.2 +/- 1.9 ml/min per 100 ml, respectively, in normal subjects, p = NS). After administration of L-NMMA in the brachial artery, forearm blood flows in normal subjects significantly decreased by 10% to 21% during hand grip exercise but did not change during exercise in patients with congestive heart failure.
Regional inhibition of nitric oxide synthase with administration of L-NMMA in the brachial artery significantly decreased forearm blood flows during rhythmic hand grip exercise in normal subjects but not in patients with congestive heart failure. These findings suggest that nitric oxide-mediated vasodilation during submaximal exercise is impaired in the forearm circulation of patients with congestive heart failure.
本研究旨在探讨内皮源性一氧化氮在正常受试者和充血性心力衰竭患者运动过程中对前臂血流调节的作用。
充血性心力衰竭患者外周循环中,一氧化氮介导的对毒蕈碱刺激的血管舒张作用受损。充血性心力衰竭患者运动期间一氧化氮介导的血管舒张是否也受损尚不清楚。
通过静脉阻断体积描记法,在17例充血性心力衰竭患者(平均年龄49岁,平均左心室射血分数0.22)和10例年龄匹配的正常受试者的肱动脉中给予L-NG-单甲基精氨酸(L-NMMA)以局部抑制一氧化氮合成前后,测定在最大自主收缩的15%、30%和45%进行有节律握力运动时的前臂血流量(每100ml的ml/min)。
在肱动脉给予L-NMMA之前,充血性心力衰竭患者在最大自主收缩的15%、30%和45%进行有节律握力运动时的前臂血流量略低于正常受试者,但差异无统计学意义(充血性心力衰竭患者分别为[均值±标准误]每100ml 6.8±1.0、8.5±1.0和12.9±1.7ml/min,正常受试者分别为每100ml 6.6±1.2、11.6±1.9和16.2±1.9ml/min,p=无显著性差异)。在肱动脉给予L-NMMA后,正常受试者在握力运动期间前臂血流量显著下降10%至21%,而充血性心力衰竭患者运动期间前臂血流量无变化。
在肱动脉给予L-NMMA局部抑制一氧化氮合酶,可使正常受试者在有节律握力运动期间前臂血流量显著下降,但充血性心力衰竭患者无此现象。这些发现表明,充血性心力衰竭患者前臂循环中次最大运动期间一氧化氮介导的血管舒张受损。