Cekici Leyla, Valipour Arschang, Kohansal Robab, Burghuber Otto Chris
Department of Respiratory and Critical Care Medicine, Ludwig-Boltzmann-Institute for COPD, Otto-Wagner Hospital, Vienna, Austria.
Br J Clin Pharmacol. 2009 Apr;67(4):394-402. doi: 10.1111/j.1365-2125.2009.03377.x.
To investigate short-term effects of inhaled salbutamol on haemodynamic changes and cardiovascular autonomic control.
A randomized, single-blinded, placebo-controlled study of 0.2 mg of inhaled salbutamol was conducted on 12 healthy nonsmoking volunteers with a mean age of 24 +/- 2 years at two different testing sessions. Non-invasively obtained continuous haemodynamic measurements of cardiac output, beat-to-beat arterial blood pressure, and total peripheral resistance were recorded prior to and for a total of 120 min after inhalation of the respective study drug. Continuous cardiovascular autonomic tone was recorded using power spectral analysis of heart rate and blood pressure variability. Spontaneous baroreceptor activity was assessed by the sequence method.
There were no significant changes in any of the baseline parameters between the different testing sessions. Inhalation of salbutamol caused a significant increase in cardiac output from 6.7 +/- 1.3 to 7.7 +/- 1.4 l min(-1) (P < 0.05), and a decrease in total peripheral resistance from 1076 +/- 192 to 905 +/- 172 dyne s(-1) cm(-5) (P < 0.05) within 15 min after inhalation. Moreover, salbutamol significantly increased sympathetically mediated low-frequency heart rate variability (P < 0.01), whereas parasympathetically mediated high-frequency heart rate variability decreased (P < 0.01). All changes persisted for approximately 30 min and were fully reversible at 120 min. There were no significant changes in systolic blood pressure variability or spontaneous baroreceptor activity.
Inhalation of therapeutic doses of salbutamol in healthy subjects resulted in significant haemodynamic changes and a shift of sympathovagal balance towards increased sympathetic tone in the absence of baroreceptor activation.
研究吸入沙丁胺醇对血流动力学变化及心血管自主神经控制的短期影响。
对12名平均年龄为24±2岁的健康非吸烟志愿者进行了一项随机、单盲、安慰剂对照研究,在两个不同的测试时段给予0.2mg吸入性沙丁胺醇。在吸入相应研究药物之前及之后总共120分钟内,无创连续测量心输出量、逐搏动脉血压和总外周阻力等血流动力学指标。通过心率和血压变异性的功率谱分析记录连续的心血管自主神经张力。采用序列法评估自发压力感受器活动。
不同测试时段之间的任何基线参数均无显著变化。吸入沙丁胺醇后15分钟内心输出量从6.7±1.3升/分钟显著增加至7.7±1.4升/分钟(P<0.05),总外周阻力从1076±192达因·秒/厘米⁻⁵降至905±172达因·秒/厘米⁻⁵(P<0.05)。此外,沙丁胺醇显著增加交感神经介导的低频心率变异性(P<0.01),而副交感神经介导的高频心率变异性降低(P<0.01)。所有变化持续约30分钟,在120分钟时完全可逆。收缩压变异性或自发压力感受器活动无显著变化。
在健康受试者中吸入治疗剂量的沙丁胺醇会导致显著的血流动力学变化,且在无压力感受器激活的情况下使交感迷走平衡向交感神经张力增加的方向转变。