Department of Cardiology, Erasmus Hospital, Université Libre de Bruxelles, Brussels, Belgium.
J Cardiovasc Pharmacol Ther. 2009 Dec;14(4):323-31. doi: 10.1177/1074248409350137.
In patients with hypertension, beta blockade decreases muscle sympathetic nerve activity (MSNA; micrographic technique) expressed in burst frequency (burst/min) but does not affect MSNA expressed in burst incidence (burst/100 heart beats), because reductions in blood pressure (BP) upon each diastole continue to deactivate the arterial baroreceptors, but at a slower heart rate (HR). We studied the effects of oral beta blockade on MSNA and baroreflex sensitivity (BRS) in normal participants. Bisoprolol (5 mg, 1 week) was administered in 10 healthy young adults, using a double-blind, placebo-controlled, randomized cross-over study design. The beat-to-beat mean RR interval (RR) and systolic blood pressure (SBP) series were analyzed by power spectral analysis and power computation over the very low frequency (VLF), low frequency, and high frequency (HF) bands. Baroreflex sensitivity was computed from SBP and RR cross-analysis, using time and frequency domain methods. Bisoprolol increased RR (P < .0005), decreased mean SBP and diastolic blood pressure values (P < .01), did not change the SBP and RR powers, except for RR power in VLF (P < .02) and SBP power in HF (P < .03). The MSNA variability (P > .13) and respiratory pattern (P = .84) did not change from placebo to bisoprolol condition. The bisoprolol-induced bradycardia was associated with higher burst/100 heart beats (P < .05) and bisoprolol did not affect burst/min (P = .80). Time domain BRS estimates were increased after bisoprolol (P < .05), while frequency domain ones did not change (P > .1). Oral bisoprolol induces differential effects on sympathetic burst frequency and incidence in normal participants. Peripheral sympathetic outflow over time is preserved as a result of an increased burst incidence, in the presence of a slower HR. Unchanged BP and HR and MSNA variability suggests that the larger burst incidence is not due to sympathetic activation.
在高血压患者中，β受体阻滞剂降低肌肉交感神经活动（MSNA；显微技术）的爆发频率（爆发/分钟），但不影响 MSNA 的爆发发生率（爆发/100 次心跳），因为每次舒张期的血压（BP）下降继续使动脉压力感受器失活，但心率（HR）较慢。我们研究了口服β受体阻滞剂对正常参与者的 MSNA 和压力反射敏感性（BRS）的影响。在一项双盲、安慰剂对照、随机交叉研究中，10 名健康年轻成年人接受了比索洛尔（5mg，1 周）治疗。通过功率谱分析和非常低频率（VLF）、低频和高频（HF）带的功率计算分析逐拍平均 RR 间期（RR）和收缩压（SBP）序列。使用时间和频域方法，从 SBP 和 RR 交叉分析中计算压力反射敏感性。比索洛尔增加 RR（P<.0005），降低平均 SBP 和舒张压值（P<.01），除了 RR 在 VLF（P<.02）和 SBP 在 HF（P<.03）的功率外，不改变 SBP 和 RR 功率。MSNA 变异性（P>.13）和呼吸模式（P=.84）从安慰剂到比索洛尔状态没有变化。比索洛尔引起的心动过缓与更高的爆发/100 次心跳（P<.05）有关，而爆发/分钟不受影响（P=.80）。比索洛尔后时间域 BRS 估计值增加（P<.05），而频域估计值不变（P>.1）。口服比索洛尔在正常参与者中对交感神经爆发频率和发生率产生不同的影响。由于心率较慢，爆发发生率增加，从而保持了随时间推移的外周交感神经输出。不变的 BP 和 HR 以及 MSNA 变异性表明，更大的爆发发生率不是由于交感神经激活引起的。
