© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Sympathetic activation triggers ventricular arrhythmias in rat heart with chronic infarction and failure
Alfred and Baker Medical Unit, Baker Medical Research Institute and Alfred Hospital, P.O. Box 6492, St. Kilda Road Central, Melbourne, Victoria 8008, Australia
* Corresponding author. Tel.: +613-9522-4396; fax: +613-9521-1362 xiaojun.du{at}baker.edu.au
Objective: To seek direct evidence for a cause–effect relation between sympathetic activation and arrhythmogenesis. Methods: Rats underwent open-chest surgery with either coronary artery occlusion or sham operation, and were studied 8 weeks later using in situ heart perfusion and nerve stimulation methods. Results: Infarcted rats showed cardiac functional impairment and increased heart and lung weight. The extent of these changes correlated well with infarct size (IS). In in situ perfused hearts, sympathetic nerve stimulation (2 and 4 Hz, 45 s duration) induced a frequency-dependent release of norepinephrine (NE). NE release was lower in MI than that in control groups. In hearts with large IS (
40%, n=19) ventricular arrhythmias were rare at baseline, but nerve stimulation evoked the onset of ventricular premature beats (95%), tachycardia (37%) and fibrillation (26%). IS and stimulation frequency were key determinants for the inducibility of arrhythmias. Lower K+ concentration enhanced arrhythmia inducibility. β-blockade inhibited the frequency of arrhythmias produced by nerve stimulation. Conclusion: In infarcted rat hearts sympathetic activation is a potent trigger for the onset of ventricular tachyarrhythmias.
KEYWORDS Experimental; Heart; Pathophysiology; Myocardial infarction; Heart failure; Sympathetic nervous system; Ventricular arrhythmias; Rats
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