Cardiac pacing-induced delayed protection against ventricular arrhythmias: Evidence for the role of nitric oxide

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Objective: To examine the role of nitric oxide in the delayed phase of cardioprotection induced by 'single' or repeated cardiac pacing against ventricular arrhythmias in anaesthetized dogs. Animals and methods: Mongrel dogs were paced four times for 5 mins at 220 beats/min under light pentobarbitone anaesthesia by means of a bipolar pacing electrode. Twenty-four hours later, one group of dogs (single paced group) was reanaesthetized with chloralose and urethane, and thoracotomized, and the left anterior descending coronary artery (LAD) was occluded for 25 mins followed by reperfusion. In another group, dogs were paced on day 1, and the pacing procedure was repeated 48 h later (repeatedly paced group). Sham-operated dogs served as controls and were subjected only to LAD occlusion, 24 h or 120 h after surgical interventions. To examine whether nitric oxide is involved in delayed antiarrhythmic protection, aminoguanidine (50 mg/kg intravenously) and S-(2-aminoethyl)-methylisothiourea (AEST) (2 mg/kg intravenously) were administered in single and repeatedly paced dogs, respectively. Results: Compared with controls, in dogs paced 24 h previously the number of ectopic beats, episodes of ventricular tachycardia and the incidence of ventricular fibrillation (VF) (83% versus 38%, P<0.05) were markedly reduced. Administration of aminoguanidine before either pacing or occlusion of the LAD markedly attenuated the protection against arrhythmias because the number of ectopic beats and the incidences of VF either during occlusion (50% and 34%, respectively) or after reperfusion (VF 83% and 89%, respectively) were increased. Compared with sham-operated controls, in repeatedly paced dogs the number of premature ventricular complexes and episodes of ventricular tachycardia, and the incidence of VF from combined occlusion-reperfusion insult (VF 70% versus 30%, P<0.05) were markedly decreased 72 h after the second pacing stimulus. Administration of AEST before LAD occlusion in repeatedly paced dogs abolished this marked antiarrhythmic protection (VF 87%). Conclusions: Right ventricular pacing resulted in marked delayed protection against ischemia- and reperfusion-induced ventricular arrhythmias in anaesthetized dogs. This delayed anti-arrhythmic protection was apparent 24 h after single (4x5 mins) and 72 h after repeated (4x5 mins on day 1 and day 3) cardiac pacing. Administration of aminoguanidine and AEST, selective inhibitors of inducible nitric oxide synthase, markedly attenuated or even abolished the protection against ventricular arrhythmias. This indicates that nitric oxide is involved, most probably through generation of inducible nitric oxide synthase, in this delayed cardioprotection.

Original languageEnglish
Pages (from-to)17-23
Number of pages7
JournalExperimental and Clinical Cardiology
Issue number1
Publication statusPublished - Jan 1 2000



  • Cardioprotection
  • Dog
  • Nitric oxide
  • Ventricular arrhythmia

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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