Cervical spinal modulation of vagal and sympathetic outflows to the ischemic heart: adverse vs cardioprotective effects

Abstract

High cervical spinal neurons modulate the responsiveness of afferent and efferent cardiac control.Objective: To determine whether high cervical spinal neurons exert differential effects on cardiac myocyte viability and electrical stability during ischemia.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 1) neuroaxis intact, 2) SCS following bilateral cervical vagotomy, and 3) SCS following muscarinic or selective adrenergic blockade. Infarct size (IS), measured by tetrazolium, was expressed as percentage of risk zone.Results: SCS reduced infarct size by 43% without increasing the incidence of sudden cardiac death (SCD). Alpha or beta adrenergic blockade returned infarct size to sham levels. Beta blockade eliminated ischemia induced ventricular fibrillation; alpha blockade doubled the incidence of sudden cardiac death. SCS mediated cardioprotection against cell death was preserved following vagotomy; it was abolished by atropine. In the presence of SCS, sudden cardiac death was eliminated by vagotomy but unaffected by atropine.Conclusions: Central neuronal influence on infarct size does not parallel that of sudden cardiac death. These data point to the underlying differential control of high cervical neurons on sympathetic and parasympathetic cardiac efferent neurons. (Supported by HL71830)