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右美托咪定对动脉心脏压力反射功能的影响:通过频谱和传递函数分析评估。

The effect of dexmedetomidine on arterial-cardiac baroreflex function assessed by spectral and transfer function analysis.

机构信息

Division of Anesthesiology, Department of Anesthesiology, Nihon University School of Medicine, Tokyo, Japan.

出版信息

J Anesth. 2012 Aug;26(4):483-9. doi: 10.1007/s00540-012-1363-0. Epub 2012 Mar 2.

Abstract

PURPOSE

The α(2)-adrenergic receptor agonist dexmedetomidine reportedly weakens heart rate (HR) responses to 'rapid' (during a few seconds) reduction in arterial pressure, but does not affect HR responses to 'gradual' (during 60 s) reduction in arterial pressure. As the speed of neurotransmission along the parasympathetic nerve is relatively rapid, alteration of parasympathetic-mediated arterial-cardiac baroreflex function plays a more important role in HR responses to 'rapid' changes in arterial pressure. We therefore hypothesized that dexmedetomidine attenuates parasympathetic-mediated arterial-cardiac baroreflex function.

METHODS

Twelve healthy men received placebo, low-dose (loading, 3 μg/kg/h for 10 min; maintenance, 0.2 μg/kg/h for 60 min) (low-DEX), or moderate-dose (loading, 6 μg/kg/h for 10 min; maintenance, 0.4 μg/kg/h for 60 min) (moderate-DEX) dexmedetomidine infusions in a randomized, double-blind, crossover study. Before and after 70 min of infusion, arterial-cardiac baroreflex function was assessed by spectral and transfer function analysis between arterial pressure variability and HR variability.

RESULTS

The high-frequency power of systolic arterial pressure (SAP) variability increased significantly with low-DEX and moderate-DEX infusions (significant interaction effects, P = 0.005), whereas the high-frequency power of R-wave-R-wave interval (RRI) variability (as an index of cardiac parasympathetic activity) did not change significantly at any dose infusions. Then, transfer function gain in the high-frequency range (as an index of parasympathetic arterial-cardiac baroreflex) decreased significantly with low-DEX and moderate-DEX infusions (significant interaction effects, P = 0.007).

CONCLUSIONS

The present results suggest that dexmedetomidine attenuates parasympathetic-mediated arterial-cardiac baroreflex function, implying weakened HR response to 'rapid' reduction in arterial pressure.

摘要

目的

据报道,α(2)-肾上腺素受体激动剂右美托咪定可减弱心率(HR)对动脉压“快速”(在几秒钟内)降低的反应,但不影响 HR 对动脉压“逐渐”(在 60 秒内)降低的反应。由于沿着副交感神经的神经传递速度相对较快,因此副交感神经介导的动脉心脏压力反射功能的改变在 HR 对动脉压“快速”变化的反应中起着更重要的作用。因此,我们假设右美托咪定可减弱副交感神经介导的动脉心脏压力反射功能。

方法

12 名健康男性接受安慰剂、低剂量(负荷量 3μg/kg/h 持续 10 分钟;维持量 0.2μg/kg/h 持续 60 分钟)(低剂量右美托咪定)或中剂量(负荷量 6μg/kg/h 持续 10 分钟;维持量 0.4μg/kg/h 持续 60 分钟)(中剂量右美托咪定)的右美托咪定输注,采用随机、双盲、交叉研究。在输注 70 分钟前后,通过动脉压变异性与 HR 变异性之间的谱和传递函数分析评估动脉心脏压力反射功能。

结果

低剂量右美托咪定和中剂量右美托咪定输注后,收缩压变异性的高频功率显著增加(交互作用效应显著,P=0.005),而 R 波-R 波间期(RRI)变异性的高频功率(作为心脏副交感神经活动的指标)在任何剂量输注时均无显著变化。然后,高频范围内的传递函数增益(作为副交感神经动脉心脏压力反射的指标)随着低剂量右美托咪定和中剂量右美托咪定的输注而显著降低(交互作用效应显著,P=0.007)。

结论

本研究结果表明,右美托咪定可减弱副交感神经介导的动脉心脏压力反射功能,这意味着 HR 对动脉压“快速”降低的反应减弱。

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