Relative attenuation of sympathetic drive during exercise in patients with congestive heart failure.
Relative attenuation of sympathetic drive during exercise in patients with congestive heart failure.
复制标题
充血性心力衰竭患者运动期间交感神经驱动的相对减弱。
DOI：
10.1016/s0735-1097(85)80420-4
复制
发表时间：
1985
影响因子：
24
通讯作者：
Cohn,JN
中科院分区：
文献类型：
--
作者：
Francis,GS;Goldsmith,SR;Ziesche,S;Nakajima,H;Cohn,JN
充血性心力衰竭患者被认为在休息时和动态运动期间交感神经驱动力增强。运动期间观察到的增强可能与心力衰竭患者在相对较低的工作负荷下经历的近乎疲惫的状态有关。为了比较正常受试者和心力衰竭患者在可比较的生理参考框架下工作时交感神经系统对运动的反应，两组的数据可以表示为达到的峰值耗氧量百分比（峰值摄氧量百分比），而不是绝对耗氧量 (VO2) 的函数。 在直立最大自行车运动期间，对 10 名健康对照受试者和 31 名患有慢性临床 II 级和 III 级心力衰竭的患者进行了研究。 31 名患者中有 18 名患有原发性心肌病，13 名患有缺血性心肌病。心力衰竭组的静息时平均射血分数为 24 ± 10% (±SD)。在休息和运动过程中测量心率、收缩压、摄氧量和血浆去甲肾上腺素水平。当数据表示为达到峰值摄氧量百分比的函数时，心力衰竭患者的血浆去甲肾上腺素对运动的反应比正常人表现出更平坦的斜率（p = 0.004），表明交感神经驱动力相对减弱。这伴随着心率（p = 0.001）和血压（p < 0.001）反应减弱。当数据表示为绝对摄氧量的函数时，这些差异并不明显。因此，当使用可比的生理参考框架进行比较时，心力衰竭患者在运动期间交感神经驱动可能相对减弱而不是增强。交感神经驱动力降低可能部分解释了心率和血压对运动反应迟钝的原因，并且与更广泛的假设相一致，即心力衰竭的特征是尽管基础状态下交感神经驱动力增加，但各种刺激普遍无法最大限度地激活交感神经系统。
Patients with congestive heart failure have been considered to have augmented sympathetic drive both at rest and during dynamic exercise. The augmentation observed during exercise may be related to the state of near exhaustion experienced by patients with heart failure at relatively low work loads. To compare the response of the sympathetic nervous system to exercise in normal subjects and patients with heart failure when they are working in a comparable physiologic frame of reference, the data for both groups can be expressed as percent peak oxygen consumption achieved (percent peak VO2) rather than as a function of absolute oxygen consumption (VO2).Ten healthy control subjects and 31 patients with chronic clinical class II and III heart failure were studied during upright maximal bicycle exercise. Eighteen of the 31 patients had primary cardiomyopathy and 13 had ischemic cardiomyopathy. The average ejection fraction at rest was 24 ± 10% (±SD) in the group with heart failure. Heart rate, systolic blood pressure, VO2and plasma norepinephrine levels were measured at rest and throughout exercise. When the data were expressed as a function of percent peak VO2 achieved, patients with heart failure demonstrated a flatter slope (p = 0.004) than normal in the response of plasma norepinephrine to exercise, indicating a relative blunting of sympathetic drive. This was accompanied by attenuated heart rate (p = 0.001) and blood pressure (p < 0.001) responses. These differences were not apparent when the data are expressed as a function of absolute VO2.Thus, patients with heart failure may have a relative attenuation rather than augmentation of sympathetic drive during exercise when comparisons are made using a comparable physiologic frame of reference. Reduced sympathetic drive might partially explain the blunted heart rate and blood pressure responses to exercise and is consistent with the broader hypothesis that heart failure is characterized by a generalized inability of various stimuli to maximally activate the sympathetic nervous system despite increased sympathetic drive in the basal state.