title: Modulation of intrinsic cardiac neurons by spinal cord stimulation: implications for its therapeutic use in angina pectoris.
abstract: OBJECTIVE
  Electrical stimulation of the dorsal aspect of the upper thoracic spinal cord is used increasingly to treat patients with severe angina pectoris refractory to conventional therapeutic strategies. Clinical studies show that spinal cord stimulation (SCS) is a safe adjunct therapy for cardiac patients, producing anti-anginal as well as anti-ischemic effects. However, little information is yet available about the underlying mechanisms involved.
  
  
  METHODS
  In order to determine its mechanism of action, the effects of SCS on the final common integrator of cardiac function, the intrinsic cardiac nervous system, was studied during basal states as well as during transient (2 min) myocardial ischemia. Activity generated by intrinsic cardiac neurons was recorded in 9 anesthetized dogs in the absence and presence of myocardial ischemia before, during and after stimulating the dorsal T1-T2 segments of the spinal cord at 66 and 90% of motor threshold using epidural bipolar electrodes (50 Hz; 0.2 ms; parameters within the therapeutic range used in humans).
  
  
  RESULTS
  The SCS suppressed activity generated by intrinsic cardiac neurons. No concomitant change in monitored cardiovascular indices was detected. Neuronal activity increased during transient ventricular ischemia (46%), as well as during the early reperfusion period (68% compared to control). Despite that, activity was suppressed during both states by SCS.
  
  
  CONCLUSIONS
  SCS modifies the capacity of intrinsic cardiac neurons to generate activity. SCS also acts to suppress the excitatory effects that local myocardial ischemia exerts on such neurons. Since no significant changes in monitored cardiovascular indices were observed during SCS, it is concluded that modulation of the intrinsic cardiac nervous system might contribute to the therapeutic effects of SCS in patients with angina pectoris.
authors.affiliation: Department of Physiology, OUHSC, Oklahoma City, OK 73190, USA.
authors.forename: R D
authors.initials: RD
authors.lastname: Foreman
authors.forename: B
authors.initials: B
authors.lastname: Linderoth
authors.forename: J L
authors.initials: JL
authors.lastname: Ardell
authors.forename: K W
authors.initials: KW
authors.lastname: Barron
authors.forename: M J
authors.initials: MJ
authors.lastname: Chandler
authors.forename: S S
authors.initials: SS
authors.lastname: Hull
authors.forename: G J
authors.initials: GJ
authors.lastname: TerHorst
authors.forename: M J
authors.initials: MJ
authors.lastname: DeJongste
authors.forename: J A
authors.initials: JA
authors.lastname: Armour
mesh_terms: D000200:Action Potentials; D000787:Angina Pectoris / Q000628:therapy*; D000818:Animals; D001341:Autonomic Nervous System; D004285:Dogs; D004599:Electric Stimulation Therapy; D006321:Heart / Q000294:innervation*; D008297:Male; D017202:Myocardial Ischemia / Q000503:physiopathology* / Q000628:therapy; D009474:Neurons / Q000502:physiology; D011897:Random Allocation; D012815:Signal Processing, Computer-Assisted; D013116:Spinal Cord