title: Cardiovascular indices of peripheral and central sympathetic activation.
abstract: 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 beta-sympathetic stimulation and blockade were achieved with epinephrine and esmolol hydrochloride (beta1-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 Hg(2), p =.03) and decreased during norepinephrine infusion (-0.67 +/- 0.13 ln mm Hg(2), 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.
authors.affiliation: Department of Internal Medicine, Division of Psychosomatic Medicine, University Hospital, Basel, Switzerland. Harmut.Schaechinger@unibas.ch
authors.forename: H
authors.initials: H
authors.lastname: Schächinger
authors.forename: M
authors.initials: M
authors.lastname: Weinbacher
authors.forename: A
authors.initials: A
authors.lastname: Kiss
authors.forename: R
authors.initials: R
authors.lastname: Ritz
authors.forename: W
authors.initials: W
authors.lastname: Langewitz
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage; D000318:Adrenergic beta-Agonists / Q000008:administration & dosage; D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage; D000328:Adult; D001794:Blood Pressure / Q000187:drug effects; D002320:Cardiovascular Physiological Phenomena / Q000187:drug effects*; D002319:Cardiovascular System / Q000187:drug effects*; D018592:Cross-Over Studies; D004837:Epinephrine / Q000008:administration & dosage; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008297:Male; D009599:Nitroprusside / Q000008:administration & dosage; D009638:Norepinephrine / Q000008:administration & dosage; D011412:Propanolamines / Q000008:administration & dosage; D016037:Single-Blind Method; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000502:physiology; D014665:Vasodilator Agents / Q000008:administration & dosage
chemical_list: D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D011412:Propanolamines; D014665:Vasodilator Agents; D009599:Nitroprusside; C036604:esmolol; D009638:Norepinephrine; D004837:Epinephrine