title: Reflex control of sympathetic activity during simulated ventricular tachycardia in humans.
abstract: BACKGROUND
  Ventricular tachyarrhythmias present a unique set of stimuli to arterial and cardiopulmonary baroreceptors by increasing cardiac filling pressures and decreasing arterial pressure. The net effect on the control of sympathetic nerve activity (SNA) in humans is unknown. The purpose of this study was to determine the relative roles of cardiopulmonary and arterial baroreceptors in controlling SNA and arterial pressure during ventricular pacing in humans.
  
  
  RESULTS
  Two experiments were performed in which SNA and hemodynamic responses to ventricular pacing were compared with nitroprusside infusion (NTP) in 12 patients and studied with and without head-up tilt or phenylephrine to normalize the stimuli to either the arterial or cardiopulmonary baroreceptors in 9 patients. In experiment 1, the slope of the relation between SNA and mean arterial pressure was greater during NTP (-4.7+/-1.4 U/mm Hg) than during ventricular pacing (-3.4+/-1.1 U/mm Hg). Comparison of NTP doses and ventricular pacing rates that produced comparable hypotension showed that SNA increased more during NTP (P=0.03). In experiment 2, normalization of arterial pressure during pacing resulted in SNA decreasing below baseline (P<0.05), whereas normalization of cardiac filling pressure resulted in a greater increase in SNA than pacing alone (212+/-35% versus 189+/-37%, P=0. 04). Conclusions--These data demonstrate that in humans arterial baroreflex control predominates in mediating sympathoexcitation during ventricular tachyarrhythmias and that cardiopulmonary baroreceptors contribute significant inhibitory modulation.
authors.affiliation: Department of Integrative Physiology, University of North Texas Health Science Center, Ft Worth, Texas, USA. msmith@hsc.unt.edu
authors.forename: M L
authors.initials: ML
authors.lastname: Smith
authors.forename: J A
authors.initials: JA
authors.lastname: Joglar
authors.forename: S L
authors.initials: SL
authors.lastname: Wasmund
authors.forename: M D
authors.initials: MD
authors.lastname: Carlson
authors.forename: P J
authors.initials: PJ
authors.lastname: Welch
authors.forename: M H
authors.initials: MH
authors.lastname: Hamdan
authors.forename: K
authors.initials: K
authors.lastname: Quan
authors.forename: R L
authors.initials: RL
authors.lastname: Page
mesh_terms: D000200:Action Potentials; D000328:Adult; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects; D006328:Cardiac Catheterization; D002304:Cardiac Pacing, Artificial; D002316:Cardiotonic Agents / Q000494:pharmacology; D002317:Cardiovascular Agents / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D008875:Middle Aged; D009599:Nitroprusside / Q000494:pharmacology; D010543:Peroneal Nerve / Q000503:physiopathology; D010656:Phenylephrine / Q000494:pharmacology; D012021:Reflex, Abnormal / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013617:Tachycardia, Supraventricular / Q000503:physiopathology; D017180:Tachycardia, Ventricular / Q000503:physiopathology*; D018667:Tilt-Table Test; D014665:Vasodilator Agents / Q000494:pharmacology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
chemical_list: D002316:Cardiotonic Agents; D002317:Cardiovascular Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine