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

Citation
Mp. Tulppo et al., Effects of pharmacological adrenergic and vagal modulation on fractal heart rate dynamics, CLIN PHYSL, 21(5), 2001, pp. 515-523
Citations number
32
Categorie Soggetti
General & Internal Medicine",Physiology
Journal title
CLINICAL PHYSIOLOGY
ISSN journal
01445979 → ACNP
Volume
21
Issue
5
Year of publication
2001
Pages
515 - 523
Database
ISI
SICI code
0144-5979(200109)21:5<515:EOPAAV>2.0.ZU;2-O
Abstract
Breakdown of short-term fractal-like behaviour of HR indicates an increased risk for adverse cardiovascular events and mortality, but the pathophysiol ogical background for altered fractal HR dynamics is not known. Our aim was to study the effects of pharmacological modulation of autonomic function o n fractal correlation properties of heart rate (HR) variability in healthy subjects. Short-term fractal scaling exponent (alpha (1)) along with spectr al components of HR variability were analysed during the following pharmaco logical 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 a tropine (n=10), (v) and vagal activation by low dose of atropine (n=10). Th en alpha (1) decreased progressively during the incremental doses of NE (fr om 0.85 +/- 0.250 to 0.55 +/- 0.23, P <0.0001). NE also decreased the avera ge HR (P <0.001) and increased the high frequency spectral power (P <0.001) . Vagal blockade with atropine increased the alpha (1) value (from 0.82 +/- 0.22 to 1.24 +/- 0.41, P <0.05). Combined NE + EPI infusion and vagal acti vation with a low dose atropine did not result in any changes in alpha (1), and alpha -adrenergic blockade by PHE did not completely reverse the effec ts of NE on alpha (1). Increased levels of circulating NE result in reducti on 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.