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Are the Sympathetic Neural Effects of Digoxin and Quinidine Involved in Their Action on Cardiac Rhythm?
Journal article   Open access   Peer reviewed

Are the Sympathetic Neural Effects of Digoxin and Quinidine Involved in Their Action on Cardiac Rhythm?

Claire Lathers, Jay Roberts and James R Roberts
Journal of cardiovascular pharmacology, v 7(2), pp 350-360
Mar 1985
DOI: https://doi.org/10.1097/00005344-198503000-00022
PMID: 2581091
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://doi.org/10.1097/00005344-198503000-00022View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze),  Open

Abstract

This study was initiated to determine if ventricular arrhythmia induced by digoxin was associated with a nonuniform neural discharge in the cardiac sympathetic postganglionic fibers. In addition, splanchnic neural discharge was monitored to explore the role of adrenal medullary catecholamines in digoxin-induced arrhythmia. Experiments were performed to ascertain whether the antiarrhythmic effects of quinidine in digoxin-induced arrhythmias were related to an action on cardiac sympathetic neural discharge induced by digoxin. All cats were anesthetized with α-chloralose and given atropine; some were pretreated with quinidine (10 or 20 mg/kg i.v. 15 min before digoxin). Digoxin was given every 15 min until death; the first three doses were 50 μg/kg i.v., and all subsequent doses were 25 μg/kg. The mean ± SE time to arrhythmia was 32 ± 4 min (n = 16) and was significantly increased only after 20 mg/kg quinidine (64 ± 7 min; p < 0.001). Mean ± SE time to death was also increased from 74 ± 4 to 98 ± 7 min (p < 0.001). Postganglionic cardiac sympathetic neural discharge before digoxin-induced arrhythmia was depressed. Of the 28 nerves monitored in 16 animals receiving digoxin, in the minute before development of arrhythmia, 22 nerves were depressed, 3 were increased, and 3 showed no change when compared with the predigoxin control. Following this depression of neural discharge, arrhythmia developed, and the neural discharge began to rise, eventually increasing above control levels. During this time the variability of the neural discharge increased greatly, as evidenced by large SE values, so that the mean values were not significantly different from control levels. Splanchnic neural discharge (n = 9) progressively decreased, reaching 66% of control values after the third injection of digoxin; the discharge then began to increase gradually toward control levels in the next 10 min and arrhythmia developed. The data indicate that the arrhythmias caused by digoxin are not associated with the development of nonuniform discharge patterns in the cardiac sympathetic nerves. Furthermore, action on the splanchnic nerve discharge is not involved in the arrhythmogenic effects of digoxin. Pretreatment with quinidine, 20 mg/kg, decreased both splanchnic and postganglionic cardiac sympathetic neural discharge, arterial blood pressure, and heart rate. Although quinidine. 20 mg/kg, increased the time to arrhythmia induced by digoxin, the depression of postganglionic cardiac or splanchnic neural discharge did not seem to be a major component of the antiarrhythmic effect of quinidine.

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Web of Science research areas
Cardiac & Cardiovascular Systems
Pharmacology & Pharmacy
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