Depressant effects of fast sodium channel blockade on the electrical activity of ischaemic canine ventricle: Mediation by the sympathetic nervous system

Robert F. Gilmour, Daryl G. Morrical, Phillip J. Ertel, John F. Maesaka, Douglas P. Zipes

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

Summary: In this study we examined the possibility that local anaesthetic agents such as tetrodotoxin may exacerbate electrical changes during acute myocardial ischaemia by inhibiting fast sodium channels, both in cardiac cells and in sympathetic nerve terminals. Bipolar electrograms were recorded during serial 2 to 5 min occlusions of the left anterior descending coronary artery in open-chest, anaesthetised dogs. Tetrodotoxin (1 or 2 μg·kg-1 iv) given prior to occlusion did not affect activation times or electrograms in normal myocardium but exacerbated activation delay and loss of electrogram amplitude during ischaemia. Bilateral stellectomy reversed the effects of tetrodotoxin during ischaemia. Tetrodotoxin (1 μg·kg-1 iv) reduced changes in heart rate and mean arterial blood pressure produced by stellate ganglia stimulation. Intracoronary infusion of tetrodotoxin (10-5 mol·litre-1) during normal perfusion lengthened mean effective ventricular refractory periods and propranolol (0.5 mg·kg-1 iv) or bilateral stellectomy prevented this effect. Thus, tetrodotoxin appeared to increase ventricular refractoriness and exacerbate ischaemia-induced activation delay by inhibiting sympathetic nerve activity. Other agents with local anaesthetic properties may have similar effects.

Original languageEnglish
Pages (from-to)405-413
Number of pages9
JournalCardiovascular Research
Volume18
Issue number7
DOIs
StatePublished - Jul 1984

Keywords

  • Ischaemia
  • Local anaesthetics
  • Sodium channels
  • Sympathetic nervous system

ASJC Scopus subject areas

  • Statistics, Probability and Uncertainty
  • Applied Mathematics
  • Physiology (medical)
  • Physiology
  • Cardiology and Cardiovascular Medicine

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