Preemptive, but not reactive, spinal cord stimulation mitigates transient ischemia-induced myocardial infarction via cardiac adrenergic neurons

E. M. Southerland, D. M. Milhorn, R. D. Foreman, B. Linderoth, M. J. L. DeJongste, J. A. Armour, V. Subramanian, M. Singh, K. Singh, J. L. Ardell*

*Corresponding author for this work

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    68 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)H311-H317
    Number of pages7
    JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
    Volume292
    Issue number1
    DOIs
    Publication statusPublished - 1-Jan-2007

    Keywords

    • alpha(1)-adrenoceptor
    • beta-adrenoceptor
    • ventricular infarction
    • neuromodulation
    • ANGINA-PECTORIS
    • RABBIT
    • NOREPINEPHRINE
    • CATECHOLAMINES
    • ACTIVATION
    • PROTECTION
    • ADENOSINE
    • OCCLUSION
    • RELEASE
    • TRIALS

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