Inter‐segmental spinal interactions, but not vagal projections, mediate spinal cord stimulation (SCS) induced cardioprotection to transient myocardial ischemia

Activation of C1‐C2 spinal neurons modulates responsiveness of high thoracic spinal neurons to noxious cardiac stimuli. Objective: Since neuro‐modulation of high thoracic spinal neurons reduces the size of infarcts induced by transient myocardial ischemia, we sought to determine whether C1‐C2 SCS does the same and, if so, whether such protection involves inter‐segmental spinal cord interconnections. Methods : The hearts of anesthetized rabbits, subjected to 30 min of LAD coronary arterial occlusion (CAO) followed by 3 hr of reperfusion (control), were compared to those with pre‐emptive SCS (starting 15 min prior to and continuing throughout the 30 min CAO). For SCS, the dorsal aspect of the C1‐C2 spinal cord was stimulated electrically (50 Hz; 0.2 ms; 90% of motor threshold). For pre‐emptive SCS, separate groups of animals were compared with spinal cord intact, SCS following bilateral cervical vagotomy or SCS following bilateral transection of the dorsal columns at C6. Infarct size (IS), measured by tetrazolium, was expressed as percentage of risk zone.Results: In controls exposed to 30 min of CAO, IS was 41±6% (±SD). C1‐C2 SCS reduced IS to 26±11% (p<0. 01). While SCS‐induced cardioprotection was unaffected by vagotomy (IS 24±11%), transection of the spinal cord dorsal column’s at C6 eliminated it (IS 40±8%). Conclusions : The C1‐C2 region may function as a descending controller of upper thoracic spinal reflex integration, thereby contributing to neuronal regulation of the ischemic myocardium. (HL71830)