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Cardiovascular Indices of Peripheral and Central Sympathetic Activation

Schächinger, Hartmut MD; Weinbacher, Markus MD; Kiss, Alexander MD; Ritz, Rudolf MD; Langewitz, Wolf MD

Original Articles

Objective A number of sympathetic nervous system (SNS) parameters have been used in cardiovascular psychophysiology. This study aimed to describe the pattern and redundancy of a set of SNS parameters during peripherally induced changes of cardiac sympathetic activation and reflex modulation of central SNS control. Preejection period (PEP) was assessed as a marker of peripheral sympathetic activation. Low-frequency blood pressure variability (BPV) was assessed as an estimate of central SNS control.

Methods Peripheral β-sympathetic stimulation and blockade were achieved with epinephrine and esmolol hydrochloride1-blockade), respectively. Changes in central SNS output were induced by loading and unloading arterial baroreceptors with norepinephrine and nitroprusside sodium, respectively. This single-blinded, crossover study in 24 healthy men also included two placebo control periods. PEP was derived from impedance cardiography and adjusted individually for heart rate. BPV was calculated by power spectral analyses of beat-to-beat heart rate and systolic blood pressure (Finapres system) data.

Results PEP decreased during epinephrine infusion (−40.1 ± 3.8 ms, p < .0001) and increased during esmolol infusion (+6.6 ± 3.5 ms, p = .05). PEP was shortened after central SNS activation by nitroprusside (−16.8 ± 2.9 ms, p < 0.0001). Systolic BPV in the low-frequency range (0.07–0.14 Hz, Mayer waves) increased during nitroprusside infusion (+0.44 ± 0.19 ln mm Hg2, p = .03) and decreased during norepinephrine infusion (−0.67 ± 0.13 ln mm Hg2, p < 0.0001). Low-frequency BPV did not change significantly during epinephrine or esmolol infusion.

Conclusions Our data provide empirical evidence of separable peripheral and central sympathetic response components. The combined report of low-frequency BPV and PEP gives distinct information on both central SNS control and the level of sympathetic cardiac activation achieved.

From the Department of Internal Medicine (H.S., M.W., A.K., R.R., W.L.), Division of Psychosomatic Medicine, University Hospital, Basel, Switzerland.

Received for publication June 14, 1999;

revision received January 31, 2001.

Address reprint requests to: Hartmut Schächinger, MD, Department of Internal Medicine, Division of Psychosomatic Medicine, University Hospital, Petersgraben 4, 4031 Basel, Switzerland. Email:

Copyright © 2001 by American Psychosomatic Society
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