Abstract

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 can do the same. 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) delivered to C8-T2 or C1-C2 spinal segments. For SCS, the dorsal aspect of the spinal cord was stimulated electrically (50 Hz; 0.2 ms; 90% of motor threshold). Infarct size (IS), measured by tetrazolium, was expressed as percentage of risk zone. Results In controls exposed to 30 min of CAO, IS was 36.7±9.5% (±SD). C1-C2 SCS reduced IS to 21.6±10.0% (p<0.001). C8-T2 SCS reduced IS to 21.6±6.8% (p<0.001). SCS did not alter blood pressure, including the hypotension induced by ischemia/reperfusion. The C1-C2 SCS group exhibited a 7.4 beat/min (p<0.006) increase in heart rate during CAO, an effect not present in controls or during C8-T2 SCS. Conclusions Pre-emptive SCS reduces the size of infarcts induced by transient CAO. The C1-C2 region may function as a descending controller of upper thoracic spinal reflex integration, thereby contributing to neuronal regulation of regional cardiac function. (HL71830)

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