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Am J Physiol Heart Circ Physiol 292: H311-H317, 2007. First published August 18, 2006; doi:10.1152/ajpheart.00087.2006
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Preemptive, but not reactive, spinal cord stimulation mitigates transient ischemia-induced myocardial infarction via cardiac adrenergic neurons

E. M. Southerland,1 D. M. Milhorn,1 R. D. Foreman,2 B. Linderoth,2,3 M. J. L. DeJongste,4 J. A. Armour,5 V. Subramanian,6 M. Singh,6 K. Singh,6 and J. L. Ardell1

1Department of Pharmacology, East Tennessee State University, Johnson City, Tennessee; 2Department of Physiology, Oklahoma University Health Science Center, Oklahoma City, Oklahoma; 3Department of Neurosurgery, Karolinska Institutet, Stockholm, Sweden; 4Department of Cardiology, Thorax Center, University Hospital of Groningen, Groningen, The Netherlands; 5Department of Pharmacology, Faculty of Medicine, University of Montreal, Montreal, Quebec, Canada; and 6Department of Physiology, East Tennessee State University, Johnson City, Tennessee

Submitted 21 January 2006 ; accepted in final form 7 August 2006

Our objective was to determine whether electrical neuromodulation using spinal cord stimulation (SCS) mitigates transient ischemia-induced ventricular infarction and, if so, whether adrenergic neurons are involved in such cardioprotection. The hearts of anesthetized rabbits, subjected to 30 min of left anterior descending coronary arterial occlusion (CAO) followed by 3 h of reperfusion (control), were compared with those with preemptive SCS (starting 15 min before and continuing throughout the 30-min CAO) or reactive SCS (started at 1 or 28 min of CAO). For SCS, the dorsal C8-T2 segments of the spinal cord were stimulated electrically (50 Hz, 0.2 ms, 90% of motor threshold). For preemptive SCS, separate groups of animals were pretreated 15 min before SCS onset with 1) vehicle, 2) prazosin ({alpha}1-adrenoceptor blockade), or 3) timolol (beta-adrenoceptor blockade). Infarct size (IS), measured with tetrazolium, was expressed as a percentage of risk zone. In controls exposed to 30 min of CAO, IS was 36.4 ± 9.5% (SD). Preemptive SCS reduced IS to 21.8 ± 6.8% (P < 0.001). Preemptive SCS-mediated infarct reduction was eliminated by prazosin (36.6 ± 8.8%) and blunted by timolol (29.4 ± 7.5%). Reactive SCS did not reduce IS. SCS increased phosphorylation of cardiac PKC. SCS did not alter blood pressure or heart rate. We conclude that preemptive SCS reduces the size of infarcts induced by transient CAO; such cardioprotection involves cardiac adrenergic neurons.

{alpha}1-adrenoceptor; beta-adrenoceptor; ventricular infarction; neuromodulation


Address for reprint requests and other correspondence: J. L. Ardell, Dept. of Pharmacology, East Tennessee State Univ., James H. Quillen College of Medicine, Johnson City, TN 37614-0577 (e-mail: ardellj{at}etsu.edu)




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