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Pre‐emptive C1‐C2 spinal cord stimulation (SCS) mitigates transient ischemia‐induced myocardial infarction
Author(s) -
Ardell Jeffrey L.,
Southerland E. Marie,
Smith Brooks,
Foreman Robert D.,
Armour J. Andrew
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1206-a
Subject(s) - medicine , spinal cord , anesthesia , cardiology , stimulation , reflex , ischemia , heart rate , occlusion , myocardial infarction , coronary occlusion , blood pressure , psychiatry
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)