Effects of pharmacological adrenergic and vagal modulation on fractal heart rate dynamics

• DOI: 10.1046/j.1365-2281.2001.00344.x
• Publication Date: 2003-03-11T13:37:02Z
• Authors: Mikko P. Tulppo; Timo H. Mäkikallio; Tapio Seppänen; Kevin Shoemaker; Elli Tutungi; Richard L. Hughson; Heikki V. Huikuri
• Keywords: Adult; Atropine; Male; Epinephrine; atropine; 610; Autonomic Nervous System; Norepinephrine; 03 medical and health sciences; 0302 clinical medicine; Heart Rate; Humans; Phentolamine; Adrenergic alpha-Antagonists; adrenaline; heart rate variability; Nerve Block; Vagus Nerve; Kinesiology; 3. Good health; Drug Combinations; Fractals; noradrenaline; Adrenergic Fibers; Adrenergic alpha-Agonists

Breakdown of short‐term fractal‐like behaviour of HR indicates an increased risk for adverse cardiovascular events and mortality, but the pathophysiological background for altered fractal HR dynamics is not known. Our aim was to study the effects of pharmacological modulation of autonomic function on fractal correlation properties of heart rate (HR) variability in healthy subjects. Short‐term fractal scaling exponent (α1) along with spectral components of HR variability were analysed during the following pharmacological interventions in healthy subjects: (i) noradrenaline (NE) infusion (n=22), (ii) NE infusion after phentolamine (PHE) (n=8), (iii) combined NE + adrenaline (EPI) infusion (n=12), (iv) vagal blockade with high dose of atropine (n=10), (v) and vagal activation by low dose of atropine (n=10). Then α1 decreased progressively during the incremental doses of NE (from 0·85 ± 0·250 to 0.55 ± 0·23, P<0·0001). NE also decreased the average HR (P<0·001) and increased the high frequency spectral power (P<0·001). Vagal blockade with atropine increased the α1 value (from 0·82 ± 0·22 to 1·24 ± 0·41, P<0·05). Combined NE + EPI infusion and vagal activation with a low dose atropine did not result in any changes in α1, and α‐adrenergic blockade by PHE did not completely reverse the effects of NE on α1. Increased levels of circulating NE result in reduction of short‐term correlation properties of HR dynamics. The results suggest that coactivation of cardiac vagal outflow at the time of high levels of a circulating sympathetic transmitter explains the breakdown of fractal‐like behaviour of human HR dynamics.