Taylor J A, Carr D L, Myers C W, Eckberg D L
Department of Internal Medicine, Hunter Holmes McGuire Department of Veterans Affairs Medical Center, and Medical College of Virginia, Virginia Commonwealth University, Richmond, USA.
Circulation. 1998 Aug 11;98(6):547-55. doi: 10.1161/01.cir.98.6.547.
Survival of post-myocardial infarction patients is related inversely to their levels of very-low-frequency (0.003 to 0.03 Hz) RR-interval variability. The physiological basis for such oscillations is unclear. In our study, we used blocking drugs to evaluate potential contributions of sympathetic and vagal mechanisms and the renin-angiotensin-aldosterone system to very-low-frequency RR-interval variability in 10 young healthy subjects.
We recorded RR intervals and arterial pressures during three separate sessions, with the patient in supine and 40 degree upright tilt positions, during 20-minute frequency (0.25 Hz) and tidal volume-controlled breathing after intravenous injections: saline (control), atenolol (0.2 mg/kg, beta-adrenergic blockade), atropine sulfate (0.04 mg/kg, parasympathetic blockade), atenolol and atropine (complete autonomic blockade), and enalaprilat (0.02 mg/kg, ACE blockade). We integrated fast Fourier transform RR-interval spectral power at very low (0.003 to 0.03 Hz), low (0.05 to 0. 15 Hz), and respiratory (0.2 to 0.3 Hz) frequencies. Beta-adrenergic blockade had no significant effect on very-low- or low-frequency RR-interval power but increased respiratory frequency power 2-fold. ACE blockade had no significant effect on low or respiratory frequency RR-interval power but modestly (approximately 21%) increased very-low-frequency power in the supine (but not upright tilt) position (P<0.05). The most profound effects were exerted by parasympathetic blockade: Atropine, given alone or with atenolol, abolished nearly all RR-interval variability and decreased very-low-frequency variability by 92%.
Although very-low-frequency heart period rhythms are influenced by the renin-angiotensin-aldosterone system, as low and respiratory frequency RR-interval rhythms, they depend primarily on the presence of parasympathetic outflow. Therefore the prognostic value of very-low-frequency heart period oscillations may derive from the fundamental importance of parasympathetic mechanisms in cardiovascular health.
心肌梗死后患者的生存率与其极低频（0.003至0.03赫兹）RR间期变异性水平呈负相关。这种振荡的生理基础尚不清楚。在我们的研究中，我们使用阻断药物来评估交感神经和迷走神经机制以及肾素 - 血管紧张素 - 醛固酮系统对10名年轻健康受试者极低频RR间期变异性的潜在贡献。
我们在三个不同的时段记录RR间期和动脉压，患者分别处于仰卧位和40度直立倾斜位，在静脉注射后进行20分钟的频率（0.25赫兹）和潮气量控制呼吸：生理盐水（对照）、阿替洛尔（0.2毫克/千克，β-肾上腺素能阻断）、硫酸阿托品（0.04毫克/千克，副交感神经阻断）、阿替洛尔和阿托品（完全自主神经阻断）以及依那普利拉（0.02毫克/千克，ACE阻断）。我们对极低频（0.003至0.03赫兹）、低频（0.05至0.15赫兹）和呼吸频率（0.2至0.3赫兹）的快速傅里叶变换RR间期频谱功率进行积分。β-肾上腺素能阻断对极低频或低频RR间期功率无显著影响，但使呼吸频率功率增加了2倍。ACE阻断对低频或呼吸频率RR间期功率无显著影响，但在仰卧位（而非直立倾斜位）适度增加了极低频功率（约21%）（P<0.05）。副交感神经阻断产生的影响最为显著：单独使用或与阿替洛尔联合使用阿托品，几乎消除了所有RR间期变异性，并使极低频变异性降低了92%。
尽管极低频心动周期节律受肾素 - 血管紧张素 - 醛固酮系统影响，与低频和呼吸频率RR间期节律一样，但它们主要依赖于副交感神经传出的存在。因此，极低频心动周期振荡的预后价值可能源于副交感神经机制在心血管健康中的根本重要性。
