Low-frequency component of the heart rate variability spectrum: a poor marker of sympathetic activity
Low-frequency component of the heart rate variability spectrum: a poor marker of sympathetic activity
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DOI：
10.1152/ajpheart.1999.276.1.h215
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发表时间：
1999-01-01
影响因子：
4.8
通讯作者：
Billman, GE
中科院分区：
文献类型：
--
作者：
Houle, MS;Billman, GE
心率变异性频谱的低频成分(0.06-0.10赫兹)通常被用作交感神经活动的准确反映。因此，加强心脏交感神经动力的干预措施，如运动和心肌缺血，应该会引起低频功率的增加。此外，由于交感神经激活的增强与恶性心律失常的倾向增加有关，人们还可以预测，容易发生室颤的动物的低频功率比抵抗的动物更大。为了验证这些假设，在运动的最后一分钟，71只心肌梗死治愈的狗进行了2分钟的冠状动脉闭塞：43只狗有室颤(易感)，28只狗没有心律失常(抵抗性)。仅运动或缺血就能在两组动物中引起显著的心率增加，其中易感动物的心率增加幅度最大。这些心率增加被β-肾上腺素能受体阻滞剂减弱。尽管交感神经调节了心率的增加，但两组动物的低频功率都降低了，而不是增加，其中易感动物的降幅最大：运动前对照的ms(2)(抵抗)为4.0+/-0.2(易感)，ms(2)(抵抗)为2.2+/-0.2(抵抗)。以类似的方式，副交感神经拮抗剂硫酸阿托品引起低频功率显着降低。虽然没有直接记录交感神经活动，但这些数据表明，心率功率谱的低频成分可能是交感神经系统和副交感神经系统相互作用的结果，因此不能准确反映交感神经活动的变化。
The low-frequency component of the heart rate variability spectrum (0.06-0.10 Hz) is often used as an accurate reflection of sympathetic activity. Therefore, interventions that enhance cardiac sympathetic drive, e.g., exercise and myocardial ischemia, should elicit increases in the low-frequency power. Furthermore, because an enhanced sympathetic activation has been linked to an increased propensity for malignant arrhythmias, one might also predict a greater low-frequency power in animals that are susceptible to ventricular fibrillation than in resistant animals. To test these hypotheses, a 2-min coronary occlusion was made during the last minute of exercise in 71 dogs with healed myocardial infarctions: 43 had ventricular fibrillation (susceptible) and 28 did not experience arrhythmias (resistant). Exercise or ischemia alone provoked significant heart rate increases in both groups of animals, with the largest increase in the susceptible animals. These heart rate increases were attenuated by beta-adrenergic receptor blockade. Despite the sympathetically mediated increases in heart rate, the low-frequency power decreased, rather than increased, in both groups, with the largest decrease again in the susceptible animals: 4.0 +/- 0.2 (susceptible) vs. 4.1 +/- 0.2 In ms(2) (resistant) in preexercise control and 2.2 +/- 0.2 (susceptible) vs. 2.9 +/- 0.2 In ms(2) (resistant) at highest exercise level. In a similar manner the parasympathetic antagonist atropine sulfate elicited significant reductions in the low-frequency power. Although sympathetic nerve activity was not directly recorded, these data suggest that the low-frequency component of the heart rate power spectrum probably results from an interaction of the sympathetic and parasympathetic nervous systems and, as such, does not accurately reflect changes in the sympathetic activity.