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LETTERS TO THE EDITOR

Acute Vagotomy Activates the Cholinergic Anti-Inflammatory Pathway

Academic Medical Center
Experimental Internal Medicine
Amsterdam 1100 DD, The Netherlands

ABSTRACT

Within minutes of acute myocardial infarction (MI), proinflammatory cytokines increase in the brain, heart, and plasma. We hypothesized that cardiac afferent nerves stimulated by myocardial injury signal the brain to increase central cytokines. Urethane-anesthetized male Sprague-Dawley rats underwent ligation of the left anterior descending coronary artery (LAD) or sham LAD ligation after bilateral cervical vagotomy, sham vagotomy, or application of a 10% phenol solution to the epicardial surface of the myocardium at risk. MI caused a significant increase in tumor necrosis factor (TNF)- and interleukin (IL)-1 in the plasma and heart, which was blunted by vagotomy. MI also caused a significant increase in hypothalamic TNF- and IL-1, which was not affected by vagotomy. In contrast, epicardial phenol blocked MI-induced increases in hypothalamic TNF- and IL-1 without affecting increases in the plasma and heart. These findings demonstrate that the appearance of proinflammatory cytokines in the brain after MI is independent of blood-borne cytokines and suggest that cardiac sympathetic afferent nerves activated by myocardial ischemia signal the brain to increase cytokine production. In addition, an intact vagus nerve is required for the full expression of proinflammatory cytokines in the injured myocardium and in the circulation. We conclude that the sympathetic and parasympathetic innervation of the heart both contribute to the acute proinflammatory response to MI.

REPLY

Department of Internal Medicine
Roy J. and Lucille A. Carver College of Medicine
University of Iowa and Veterans Affairs Medical Center
Iowa City, Iowa 52242

Joseph Francis

Department of Comparative Biomedical Sciences
School of Veterinary Medicine
Louisiana State University
Baton Rouge, Louisiana 70803

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