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Research Article Free access | 10.1172/JCI108908

Mechanisms Contributing to Malignant Dysrhythmias Induced by Ischemia in the Cat

Peter B. Corr, Francis X. Witkowski, and Burton E. Sobel

The Cardiovascular Division, Washington University School of Medicine, St. Louis, Missouri 63110

Find articles by Corr, P. in: JCI | PubMed | Google Scholar

The Cardiovascular Division, Washington University School of Medicine, St. Louis, Missouri 63110

Find articles by Witkowski, F. in: JCI | PubMed | Google Scholar

The Cardiovascular Division, Washington University School of Medicine, St. Louis, Missouri 63110

Find articles by Sobel, B. in: JCI | PubMed | Google Scholar

Published January 1, 1978 - More info

Published in Volume 61, Issue 1 on January 1, 1978
J Clin Invest. 1978;61(1):109–119. https://doi.org/10.1172/JCI108908.
© 1978 The American Society for Clinical Investigation
Published January 1, 1978 - Version history
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Abstract

Continuously recorded bipolar electrograms were obtained simultaneously from epi-, endo-, and mid-myocardial regions of the ischemic and normal zones of cat left ventricle in vivo after coronary occlusion, analyzed by computer, and compared to regional cyclic AMP levels. Regional cyclic AMP content was used as an index of the combined local effects of: (a) efferent sympathetic nerve discharge; (b) release of myocardial catecholamines due to ischemia; and (c) circulating catecholamines. Ischemia resulted in a progressive increase in pulse width and rise time and a decrease in rate of rise of voltage (dV/dt) of the local electrograms from ischemic zones reaching a maximum within 2.4±0.3 min (mean±SE) at the time of onset of severe ventricular dysrhythmias, all of which returned toward control before the cessation of the dysrhythmia (33.5±1.5 min after coronary occlusion). Increases in cyclic AMP in ischemic zones preceded corresponding increases in the frequency of premature ventricular complexes (PVCs). Propranolol inhibited the increases in cyclic AMP and reduced the frequency of PVCs in animals without ventricular fibrillation. In animals with ventricular fibrillation, cyclic AMP was significantly elevated in normal and ischemic zones compared to animals with PVCs only. Electrical induction of PVCs or ventricular fibrillation in ischemic and nonischemic hearts failed to increase cyclic AMP. The results suggest that the changes in regional adrenergic stimulation of the heart may contribute to perpetuation of ventricular dysrhythmia and the genesis of ventricular fibrillation early after the onset of myocardial ischemia.

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