Abstract
Myocardial ischemia frequently results in activation of the sympathetic nervous system [146], with clinical manifestations including sinus tachycardia and hypertension [158]. Of more concern than these hemodynamic alterations produced by sympathetic neural activation is the electrical instability which ensues after an ischemic event and during evolving myocardial infarction. Several lines of evidence suggest that increases in sympathetic neural activity induced by ischemia may be of primary importance in arrhythmogenesis and that stimulation of both α- and β-adrenergic receptors in the myocardium contributes to the electrophysiological derangements leading to malignant ventricular tachycardia or ventricular fibrillation resulting in sudden cardiac death. Prior to considering the electrophysiological effects of catecholamines and their relation to arrhythmogenesis in the ischemic heart, the anatomic and neurophysiological substrates underlying this relationship and the mechanisms responsible for sympathetic activation will briefly be discussed. The present review will concentrate solely on the sympathetic branch of the autonomic nervous system. The reader is referred to other reviews [31, 35] for a more detailed account of the interactions between the sympathetic and parasympathetic nervous systems.
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© 1989 Springer-Verlag Berlin Heidelberg
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Yamada, K.A., Heathers, G.P., Pogwizd, S.M., Corr, P.B. (1989). Sympathetic Influences on Arrhythmogenesis in the Ischemic Heart. In: Refsum, H., Sulg, I.A., Rasmussen, K. (eds) Heart & Brain, Brain & Heart. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-83456-1_6
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DOI: https://doi.org/10.1007/978-3-642-83456-1_6
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-642-83458-5
Online ISBN: 978-3-642-83456-1
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