Heart Institute, University of São Paulo, São Paulo, Brazil.
Hypertension. 2012 Sep;60(3):669-76. doi: 10.1161/HYPERTENSIONAHA.112.195776. Epub 2012 Jul 16.
We described recently that systemic hypoxia provokes vasoconstriction in heart failure (HF) patients. We hypothesized that either the exaggerated muscle sympathetic nerve activity and/or endothelial dysfunction mediate the blunted vasodilatation during hypoxia in HF patients. Twenty-seven HF patients and 23 age-matched controls were studied. Muscle sympathetic nerve activity was assessed by microneurography and forearm blood flow (FBF) by venous occlusion plethysmography. Peripheral chemoreflex control was evaluated through the inhaling of a hypoxic gas mixture (10% O(2) and 90% N(2)). Basal muscle sympathetic nerve activity was greater and basal FBF was lower in HF patients versus controls. During hypoxia, muscle sympathetic nerve activity responses were greater in HF patients, and forearm vasodilatation in HF was blunted versus controls. Phentolamine increased FBF responses in both groups, but the increase was lower in HF patients. Phentolamine and N(G)-monomethyl-l-arginine infusion did not change FBF responses in HF but markedly blunted the vasodilatation in controls. FBF responses to hypoxia in the presence of vitamin C were unchanged and remained lower in HF patients versus controls. In conclusion, muscle vasoconstriction in response to hypoxia in HF patients is attributed to exaggerated reflex sympathetic nerve activation and blunted endothelial function (NO activity). We were unable to identify a role for oxidative stress in these studies.
我们最近描述了系统性缺氧会引起心力衰竭（HF）患者的血管收缩。我们假设，在 HF 患者中，过度的肌肉交感神经活动和/或内皮功能障碍介导了缺氧期间血管舒张功能的减弱。我们研究了 27 名 HF 患者和 23 名年龄匹配的对照组。通过微神经记录法评估肌肉交感神经活动，通过静脉闭塞体积描记法评估前臂血流（FBF）。通过吸入低氧混合气体（10%O2 和 90%N2）评估外周化学感受器的控制。与对照组相比，HF 患者的基础肌肉交感神经活动更高，基础 FBF 更低。在缺氧期间，HF 患者的肌肉交感神经活动反应更大，HF 患者的前臂血管舒张功能减弱。苯肾上腺素增加了两组的 FBF 反应，但在 HF 患者中增加幅度较低。苯肾上腺素和 N(G)-单甲基-l-精氨酸输注并未改变 HF 中的 FBF 反应，但显著减弱了对照组的血管舒张。在存在维生素 C 的情况下，对缺氧的 FBF 反应没有改变，并且仍低于 HF 患者与对照组相比。总之，HF 患者对缺氧的血管收缩归因于过度的反射性交感神经激活和内皮功能障碍（NO 活性）。在这些研究中，我们未能确定氧化应激的作用。
