title: Effect of epivascular cardiac autonomic nerve stimulation on cardiac function.
abstract: BACKGROUND
  The cardiac plexus contains sympathetic and parasympathetic cardiac nerves. Our goal was to assess the hemodynamic and functional effects of stimulating the cardiac autonomic nervous system (CANS) at the epivascular surfaces of the cardiac plexus. Although CANS therapy to modulate cardiovascular function has drawn widespread interest, research has focused only on stimulating parasympathetic or sympathetic nerves, not both at once.
  
  
  METHODS
  Using general anesthesia and an open-chest surgical procedure, 12 dogs received epivascular stimulation of the cardiac plexus. A bipolar electrode was placed between the right pulmonary artery (PA) and the ascending aorta, with the stimulation frequency/pulse width held constant (20 Hz/4 ms) and the voltage varied (10-50 V). Left ventricular (LV) pressure-volume loops and hemodynamic data were recorded with and without stimulation.
  
  
  RESULTS
  In all dogs, aortic and LV systolic pressures, maximum rate of change of LV pressure, and LV stroke work increased (p<0.0001), as did cardiac output (2.9±1.0-0.4±1.0 L/min; p=0.001), end-systolic elastance (1.2±0.4-1.5±0.5 mm Hg/mL; p=0.0001), preload recruitable stroke work (30.1±11.0-39.3±7.8 mm Hg; p=0.003), and LV ejection fraction (p=0.012). Systemic vascular resistance increased slightly (p=0.04), and pulmonary vascular resistance decreased (p=0.01). Mean heart rate and pulmonary arterial, central venous, and left atrial pressures remained unchanged (p>0.1).
  
  
  CONCLUSIONS
  In contrast to inotropic drugs, epivascular CANS stimulation induced a significant and selective increase in LV contractility with no increase in heart rate.
authors.affiliation: Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA.
authors.forename: Mariko
authors.initials: M
authors.lastname: Kobayashi
authors.forename: Seiichiro
authors.initials: S
authors.lastname: Sakurai
authors.forename: Tohru
authors.initials: T
authors.lastname: Takaseya
authors.forename: Akira
authors.initials: A
authors.lastname: Shiose
authors.forename: Hyun-Il
authors.initials: HI
authors.lastname: Kim
authors.forename: Masako
authors.initials: M
authors.lastname: Fujiki
authors.forename: Jamshid H
authors.initials: JH
authors.lastname: Karimov
authors.forename: Raymond
authors.initials: R
authors.lastname: Dessoffy
authors.forename: Alex
authors.initials: A
authors.lastname: Massiello
authors.forename: Allen G
authors.initials: AG
authors.lastname: Borowski
authors.forename: David R
authors.initials: DR
authors.lastname: Van Wagoner
authors.forename: Eugene J
authors.initials: EJ
authors.lastname: Jung
authors.forename: Kiyotaka
authors.initials: K
authors.lastname: Fukamachi
mesh_terms: D000818:Animals; D001341:Autonomic Nervous System; D002302:Cardiac Output; D004195:Disease Models, Animal; D004285:Dogs; D004599:Electric Stimulation Therapy / Q000379:methods*; D006321:Heart / Q000294:innervation* / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology*; D006333:Heart Failure / Q000503:physiopathology / Q000628:therapy*; D009200:Myocardial Contraction; D016277:Ventricular Function, Left / Q000502:physiology*