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(Circulation Research. 2003;93:796.)
© 2003 American Heart Association, Inc.

Editorials

Sympathetic Nerves and Myocyte Necrosis

More Than Meets the Eye

John M. Canty, Jr, James A. Fallavollita

From the Veterans Affairs Western New York Health Care System and the Departments of Medicine, Physiology and Biophysics at the University at Buffalo School of Medicine and Biomedical Sciences, Buffalo, NY.

Correspondence to John M. Canty, Jr, MD, University at Buffalo, Division of Cardiology, Biomedical Research Building, Room 345, 3435 Main St, Buffalo, NY 14214. E-mail canty@buffalo.edu

Key Words: sympathetic innervation • ischemia • stunning • infarction

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The left ventricle is richly supplied with sympathetic nerves, which are spatially localized next to cardiac myocytes in a fashion that permits the rapid transmission of autonomic signals via the release of norepinephrine. Previous investigation in the heart has largely focused on the local release and reuptake kinetics of norepinephrine in conjunction with its downstream receptor-mediated events. Nevertheless, accumulating data indicate that the crosstalk between myocardial sympathetic nerves and cardiac myocytes appears to be much more complex. In addition to the co-release of other vasoactive peptides such as neuropeptide Y, sympathetic nerves can also modulate the expression of trophic factors such as nerve growth factor (NGF) and are a potential source of nitric oxide (NO) production via the neuronal NO synthase. Collectively, these can have diverse chronic effects on target tissues such as the heart, which could alter endogenous free radical scavenging mechanisms in pathophysiological states¹ as well as the expression of ion channels involved in depolarization and repolarization.² The loss of this crosstalk could alter the myocyte response to ischemia.

In this issue of Circulation Research, Huang and colleagues³ provide provocative in vivo experimental data to support the notion that the sympathetic nerves modulate oxidant-mediated injury to the heart after ischemia. Chronically instrumented swine with regional sympathetic denervation were subjected to short-term hibernation using a 40% reduction in blood flow for 90 minutes followed by reperfusion for 4 days. Although flow and function were similarly matched during ischemia, the regionally denervated heart developed greater myocardial stunning than the . . . [Full Text of this Article]