Long-term subthreshold electrical stimulation of the left stellate ganglion and a canine model of sudden cardiac death

Swissa, Moshe; Zhou, Shengmei; González-Gómez, Ignacio; Chang, Chung-Pai; Lai, Angela; Cates, Adam W.; Fishbein, Michael C.; Karagueuzian, Hrayr S.; Chen, Peng Sheng; Chen, Lan S.

doi:10.1016/j.jacc.2003.07.053

Cited by 70 publications

(62 citation statements)

References 18 publications

(29 reference statements)

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“…Sympathoexcitatory action in cervical sympathetic ganglia is induced by cardiac afferent activation [4,25,43]. Sympathoexcitatory action can exaggerate myocardial ischemia further by increasing myocardial oxygen consumption while maintaining cardiac function transiently by enhancing contractility [25,44].…”

Section: Introductionmentioning

confidence: 99%

“…Sympathoexcitatory action can exaggerate myocardial ischemia further by increasing myocardial oxygen consumption while maintaining cardiac function transiently by enhancing contractility [25,44]. Surgical interventions of sympathetic afferent pathways abolish or relieve angina pectoris [43]. Myocardial ischemia can produce a variety of chemical substances, which act on the cardiac afferent nerves.…”

Section: Introductionmentioning

confidence: 99%

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Sensory–sympathetic coupling in superior cervical ganglia after myocardial ischemic injury facilitates sympathoexcitatory action via P2X7 receptor

Peng

et al. 2013

Purinergic Signalling

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P2X receptors participate in cardiovascular regulation and disease. After myocardial ischemic injury, sensorysympathetic coupling between rat cervical DRG nerves and superior cervical ganglia (SCG) facilitated sympathoexcitatory action via P2X 7 receptor. The results showed that after myocardial ischemic injury, the systolic blood pressure, heart rate, serum cardiac enzymes, IL-6, and TNF-α were increased, while the levels of P2X 7 mRNA and protein in SCG were also upregulated. However, these alterations diminished after treatment of myocardial ischemic (MI) rats with the P2X 7 antagonist oxATP. After siRNA P2X 7 in MI rats, the systolic blood pressure, heart rate, serum cardiac enzymes, the expression levels of the satellite glial cell (SGC) or P2X 7 were significantly lower than those in MI group. The phosphorylation of ERK 1/2 in SCG participated in the molecular mechanism of the sympathoexcitatory action induced by the myocardial ischemic injury. Retrograde tracing test revealed the sprouting of CGRP or SP sensory nerves (the markers of sensory afferent fibers) from DRG to SCG neurons. The upregulated P2X 7 receptor promoted the activation of SGCs in SCG, resulting in the formation of sensory-sympathetic coupling which facilitated the sympathoexcitatory action. P2X 7 antagonist oxATP could inhibit the activation of SGCs and interrupt the formation of sensory-sympathetic coupling in SCG after the myocardial ischemic injury. Our findings may benefit the treatment of coronary heart disease and other cardiovascular diseases.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Sensory–sympathetic coupling in superior cervical ganglia after myocardial ischemic injury facilitates sympathoexcitatory action via P2X7 receptor

Peng

et al. 2013

Purinergic Signalling

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“…In normal dogs, long-term subthreshold electrical left stellate ganglia (SG) stimulation increases nerve fiber density in the heart (45). In rodents, sympathetic hyperinnervation occurs in the periinfarct area, particularly within the first week post-MI, and to a lesser extent in remote cardiac areas chronically (8,25,28,51,52).…”

mentioning

confidence: 99%

Cardiac sympathetic innervation and PGP9.5 expression by cardiomyocytes after myocardial infarction: effects of central MR blockade

Drobysheva

Ahmad

White

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Drobysheva A, Ahmad M, White R, Wang H, Leenen FH. Cardiac sympathetic innervation and PGP9.5 expression by cardiomyocytes after myocardial infarction: effects of central MR blockade. Am J Physiol Heart Circ Physiol 305: H1817-H1829, 2013. First published October 11, 2013; doi:10.1152/ajpheart.00445.2013.-Central mechanisms involving mineralocorticoid receptor (MR) activation contribute to an increase in sympathetic tone after myocardial infarction (MI). We hypothesized that this central mechanism also contributes to cardiac sympathetic axonal sprouting and that central MR blockade reduces cardiac sympathetic hyperinnervation post-MI. Post-MI, tyrosine hydroxylase (TH) and norepinephrine transporter protein content in the noninfarcted base of the heart remained unaltered. In contrast, protein gene product (PGP)9.5 protein was increased twofold in the base of the heart and sixfold in the peri-infarct area at 1 wk post-MI and was associated with increased ubiquitin expression. These changes persisted to a lesser extent at 4 wk post-MI and were no longer present at 12 wk. Cardiac myocytes rather than sympathetic axons were the main source of this elevated PGP9.5 expression. At 7-10 days post-MI, in the peri-infarct area, sympathetic hyperinnervation was observed with a fourfold increase in growth-associated protein 43, a twofold increase in TH, and a 50% increase in PGP9.5-positive fibers compared with the epicardial side of the left ventricle in sham rats. Central infusion of the MR blocker eplerenone markedly attenuated these increases in nerve densities but did not affect overall cardiac PGP9.5 and ubiquitin protein overexpression. We conclude that central MR activation contributes to sympathetic hyperinnervation, possibly by decreasing cardiac sympathetic activity post-MI, or by affecting other mechanisms, such as the expression of nerve growth factor. Marked PGP9.5 expression occurs in cardiomyocytes early post-MI, which may contribute to the increase in ubiquitin. myocardial infarction; cardiac sympathetic hyperinnervation; brain mineralocorticoid receptors; eplerenone; ubiquitin; protein gene product 9.5 CARDIAC REMODELING after myocardial infarction (MI) affects both infarcted and noninfarcted areas of the heart and contributes to the impairment of ventricular performance (19,43,44). Cardiac sympathetic hyperactivity enhances maladaptive cardiac remodeling post-MI and plays a major role in the development of chronic heart failure (CHF) (5, 31). In humans with mild CHF, there is a selective increase in cardiac sympathetic activity, which is followed by augmented sympathetic outflow to skeletal muscle and the kidneys as CHF progresses (16,38). In rats, direct recordings from cardiac sympathetic nerves demonstrate that cardiac sympathetic nerve activity (CSNA) increased twofold within hours after MI (40). In conscious sheep, CSNA was significantly increased by the second hour post-MI and remained elevated for at least 1 wk (14).Increased CSNA may also contribute to the development of cardiac sympathetic hyperi...

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“…These findings suggest that abnormally increased postinjury sympathetic nerve density may be in part responsible for the occurrence of ventricular arrhythmia and sudden cardiac death in these patients. Zhou et al 13 subsequently demonstrated that postinjury myocardial nerve sprouting and sympathetic hyperinnervation can occur after canine myocardial infarction, and that the increased magnitude of sympathetic hyperinnervation correlates with the increased incidence of VT. 10,11 These latter studies imply that excessive beta1-AR and beta2-AR activation during sympathetic discharges play a role in causing VT in this model. By serving as a buffer to the beta1-AR and beta2-AR activation, beta3-AR stimulation might reduce the effects of sympathetic activation on the diseased myocardium and thereby reduced the incidence of VT in this model.…”

Section: Effects Of Beta3-ar Stimulation On Neural Remodelingmentioning

confidence: 70%

“…We then implanted a pacemaker for back up pacing (40 bpm), and an osmotic pump (Model 2ML4, Alzet Osmotic Pumps, Cupertino, CA) for continuous infusion of NGF to LSG. For Long-term continuous ECG recordings, 11 we implanted a D70-EEE Data Sciences International (DSI) transmitter in all dogs. ECG was continuously recorded in the implanted transmitter, transmitted to RMC-1 receivers, transferred to a computer via Matrix, and automatically stored by Dataquest ART acquisition software in a hard drive for both on-line and off-line analyses.…”

Section: Surgical Procedures During First Surgerymentioning

confidence: 99%

Antiarrhythmic effects of beta3-adrenergic receptor stimulation in a canine model of ventricular tachycardia

et al. 2008

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Long-term subthreshold electrical stimulation of the left stellate ganglion and a canine model of sudden cardiac death

Abstract: Subthreshold electrical stimulation of the LSG induces cardiac nerve sprouting and sympathetic hyperinnervation and facilitates the development of a high-yield canine model of ventricular arrhythmia and SCD.

Cited by 70 publications

References 18 publications

Sensory–sympathetic coupling in superior cervical ganglia after myocardial ischemic injury facilitates sympathoexcitatory action via P2X7 receptor

Sensory–sympathetic coupling in superior cervical ganglia after myocardial ischemic injury facilitates sympathoexcitatory action via P2X7 receptor

Cardiac sympathetic innervation and PGP9.5 expression by cardiomyocytes after myocardial infarction: effects of central MR blockade

Antiarrhythmic effects of beta3-adrenergic receptor stimulation in a canine model of ventricular tachycardia

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