Dias da Silva Valdo José, Viana Públio Cesar Cavalcante, de Melo Alves Rodrigo, Fazan Rubens, Ruscone Tomaso Gnecchi, Porta Alberto, Malliani Alberto, Salgado Helio Cesar, Montano Nicola
Department of Biological Sciences, School of Medicine of Triangulo Mineiro, Uberaba (MG), Brazil.
Auton Neurosci. 2002 Jan 10;95(1-2):88-96. doi: 10.1016/s1566-0702(01)00365-4.
Amiodarone is an antiarrhythmic agent commonly used to treat cardiac arrhythmias. This study was designed to investigate the effects of intravenous amiodarone on the neural control of heart rate and arterial pressure and spontaneous baroreflex sensitivity (BRS). Experiments were carried out on conscious freely moving normotensive Wistar (WR) and spontaneously hypertensive rats (SHR). Arterial pressure was continuously monitored before and after amiodarone (50 mg/kg i.v.) or vehicle for 30 min. Heart rate (expressed as the pulse interval, PI) and systolic arterial pressure (SAP) variabilities were assessed using autoregressive spectral analysis. BRS was calculated as the alpha-index (the square root of the ratio between the PI and SAP powers). Amiodarone induced bradycardia and hypotension in both strains, with these effects being more intense in SHR. The variability profile of PI was characterized by a significant reduction of normalized low frequency (LF) and LF/HF ratio, while the high frequency (HF) component both in absolute and normalized units (nu) was increased in both WR and SHR strains. A significant decrease in SAP variance and its LF oscillation was observed. In addition, BRS was also increased in both groups, being more intense in SHR. In both WR and SHR, intravenous amiodarone had a considerable effect on heart rate variabilities (HRV), shifting cardiac sympathovagal balance toward a sympathetic inhibition and/or vagal activation, which were associated with an increase in spontaneous BRS. Decreases of SAP variance and LF(SAP) suggest sympatholytic effects on peripheral vessels. Besides the direct ion channel effects, these changes in the autonomic balance could contribute to the antiarrhythmic action of the intravenous amiodarone.
胺碘酮是一种常用于治疗心律失常的抗心律失常药物。本研究旨在探讨静脉注射胺碘酮对心率和动脉血压的神经控制以及自发性压力反射敏感性(BRS)的影响。实验在清醒自由活动的正常血压Wistar(WR)大鼠和自发性高血压大鼠(SHR)上进行。在静脉注射胺碘酮(50 mg/kg)或赋形剂前后连续监测动脉血压30分钟。使用自回归谱分析评估心率(以脉搏间期,PI表示)和收缩期动脉压(SAP)的变异性。BRS计算为α指数(PI与SAP功率之比的平方根)。胺碘酮在两种品系中均引起心动过缓和低血压,这些效应在SHR中更为强烈。PI的变异性特征是标准化低频(LF)和LF/HF比值显著降低,而WR和SHR品系中高频(HF)成分的绝对值和标准化单位(nu)均增加。观察到SAP方差及其LF振荡显著降低。此外,两组的BRS也增加,在SHR中更为强烈。在WR和SHR中,静脉注射胺碘酮对心率变异性(HRV)有相当大的影响,使心脏交感迷走神经平衡向交感抑制和/或迷走神经激活方向转变,这与自发性BRS增加有关。SAP方差和LF(SAP)的降低表明对周围血管有抗交感神经作用。除了直接的离子通道效应外,自主神经平衡的这些变化可能有助于静脉注射胺碘酮的抗心律失常作用。