title: Effects of blockade of fast and slow inward current channels on ventricular fibrillation in the pig heart.
abstract: OBJECTIVE
  To determine the contribution of fast and slow inward channels to the electrocardiogram (ECG) of ventricular fibrillation.
  
  
  METHODS
  Ventricular fibrillation was induced by endocardial electrical stimulation in pigs anaesthetised with pentobarbitone sodium (30 mg/kg intravenously). ECGs simultaneously recorded from the body surface (lead II) and from the endocardium were studied by power spectrum analysis (0-40 Hz).
  
  
  RESULTS
  The mean (SEM) dominant frequency of fibrillation (9.0 (1.1) Hz in lead II at 0-40 s) did not change significantly with time in pigs given intravenous saline. However, the dominant frequency was significantly reduced by intravenous pretreatment with the class I antiarrhythmic drugs, lignocaine (3 mg/kg, 6.5 (0.5) Hz; 10 mg/kg, 4.2 (0.6) Hz), mexiletine (3 mg/kg, 6.2 (0.4) Hz; 10 mg/kg, 5.5 (0.4) Hz), and disopyramide (2.5 mg/kg, 5.4 (0.6) Hz). After flecainide (3 mg/kg, 6.9 (0.5) Hz) the reduction in frequency was not significant. Similar data were obtained with endocardial recordings. In contrast pre-treatment with verapamil (0.2 mg/kg, 11.7 (0.8) Hz; and 1.0 mg/kg, 12.9 (1.6) Hz) produced a significantly higher dominant frequency of fibrillation than saline and widened the bandwidth of frequencies around the dominant frequency.
  
  
  CONCLUSIONS
  These results indicate that voltage-dependent sodium channel currents contribute to the rapid frequencies of ventricular fibrillation. Blockade of L-type inward calcium channel activity increases the fibrillation frequency and fractionates the frequencies of the fibrillation wavefronts.
authors.affiliation: Department of Physiology, Queen's University, Belfast.
authors.forename: A J
authors.initials: AJ
authors.lastname: Stewart
authors.forename: J D
authors.initials: JD
authors.lastname: Allen
authors.forename: A B
authors.initials: AB
authors.lastname: Devine
authors.forename: A A
authors.initials: AA
authors.lastname: Adgey
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004206:Disopyramide / Q000494:pharmacology; D004562:Electrocardiography; D005424:Flecainide / Q000494:pharmacology; D008012:Lidocaine / Q000494:pharmacology; D008801:Mexiletine / Q000494:pharmacology; D008954:Models, Biological; D000254:Sodium-Potassium-Exchanging ATPase / Q000187:drug effects / Q000378:metabolism*; D013552:Swine; D014693:Ventricular Fibrillation / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D014700:Verapamil / Q000494:pharmacology
chemical_list: D000889:Anti-Arrhythmia Agents; D002121:Calcium Channel Blockers; D008801:Mexiletine; D008012:Lidocaine; D014700:Verapamil; D000254:Sodium-Potassium-Exchanging ATPase; D004206:Disopyramide; D005424:Flecainide