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1 Pharmacology, East Tennessee State University, Johnson City, Tennessee, United States
2 Physiology, Oklahoma University Heath Science Center, Oklahoma City, Oklahoma, United States
3 Neurosurgery, Karolinska Institutet, Stockholm, Sweden
4 Cardiology, University Hospital of Groningen, Groningen, Netherlands
5 Pharmacology, University of Montreal, Montreal, Canada
6 Physiology, East Tennessee State University, Johnson City, Tennessee, United States
* To whom correspondence should be addressed. E-mail: ardellj{at}etsu.edu.
Objective. 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. 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 preemptive SCS (starting 15 min prior to and continuing throughout the 30 min CAO) or reactive SCS (started at 1 min 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 pre-emptive SCS, separate groups of animals were pretreated 15 min prior to SCS onset with 1) vehicle, 2) prazosin (
1-adrenoceptor blockade) or 3) timolol (
-adrenoceptor blockade). Infarct size (IS), measured by tetrazolium, was expressed as a percentage of risk zone. Results: In controls exposed to 30 min of CAO, IS was 36.4± 9.5% (±SD). Pre-emptive SCS reduced IS to 21.8±6.8% (p<0.001). Pre-emptive 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. Conclusions. Pre-emptive SCS reduces the size of infarcts induced by transient CAO; such cardioprotection involves cardiac adrenergic neurons.
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  J. L. Ardell, R. Cardinal, M. Vermeulen, and J. A. Armour Dorsal spinal cord stimulation obtunds the capacity of intrathoracic extracardiac neurons to transduce myocardial ischemia Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2009; 297(2): R470 - R477. [Abstract] [Full Text] [PDF]
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J. C. Hardwick, E. M. Southerland, and J. L. Ardell Chronic myocardial infarction induces phenotypic and functional remodeling in the guinea pig cardiac plexus Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2008; 295(6): R1926 - R1933. [Abstract] [Full Text] [PDF]
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X. Ding, F. Hua, K. Sutherly, J. L. Ardell, and C. A. Williams C2 spinal cord stimulation induces dynorphin release from rat T4 spinal cord: potential modulation of myocardial ischemia-sensitive neurons Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2008; 295(5): R1519 - R1528. [Abstract] [Full Text] [PDF]
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X. Ding, J. L. Ardell, F. Hua, R. J. McAuley, K. Sutherly, J. J Daniel, and C. A. Williams Modulation of cardiac ischemia-sensitive afferent neuron signaling by preemptive C2 spinal cord stimulation: effect on substance P release from rat spinal cord Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2008; 294(1): R93 - R101. [Abstract] [Full Text] [PDF]
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