title: Two types of ventricular fibrillation in isolated rabbit hearts: importance of excitability and action potential duration restitution.
abstract: BACKGROUND
  The combined effects of excitability and action potential duration (APD) restitution on wavefront dynamics remain unclear.
  
  
  RESULTS
  We used optical mapping techniques to study Langendorff-perfused rabbit hearts. In protocol IA (n=10), D600 at increasing concentrations was infused during ventricular fibrillation (VF). With concentration increased to 0.5 mg/L, fast VF (dominant frequency, 19.1+/-1.8 Hz) was consistently converted to ventricular tachycardia (VT). However, increasing D600 further to 2.5 or 5.0 mg/L converted VT to slow VF (11.9+/-2.3 Hz, P=0.0011). In an additional 4 hearts (protocol IB), tetrodotoxin converted a preexisting VT to slow VF (11.0+/-1.4 Hz). Optical maps show wandering wavelets in fast VF, organized reentry in VT, and spatiotemporal periodicity in slow VF. In protocol II, we determined APD and conduction time(-1) (CT(-1)) restitutions during D600 infusion. CT(-1) was used as an estimate of excitability. At 0.1 mg/L, APD and CT(-1) restitutions were steep and flat, respectively. APD restitution became flattened when D600 increased to 0.5 mg/L, converting fast VF to VT. Further increasing D600 to 2.5 or 5.0 mg/L steepened CT(-1) restitution and widened the range of S(1) pacing cycle lengths over which CT(-1) decreased, converting VT to slow VF.
  
  
  CONCLUSIONS
  Two types of VF exist in isolated rabbit hearts. Fast (type I) VF is associated with a steep APD restitution, a flat CT(-1) restitution, and wandering wavelets. Slow (type II) VF is associated with a flat APD restitution, a steep CT(-1) restitution, and spatiotemporal periodicity. Both excitability and APD restitution are important in VF maintenance.
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D018780:Body Surface Potential Mapping; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002304:Cardiac Pacing, Artificial; D004305:Dose-Response Relationship, Drug; D004562:Electrocardiography / Q000187:drug effects / Q000379:methods; D004567:Electrodes, Implanted; D022062:Electrophysiologic Techniques, Cardiac; D005456:Fluorescent Dyes; D005583:Fourier Analysis; D005711:Gallopamil / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D066298:In Vitro Techniques; D008027:Light; D055095:Optics and Photonics; D011726:Pyridinium Compounds; D011817:Rabbits; D026941:Sodium Channel Blockers / Q000494:pharmacology; D017180:Tachycardia, Ventricular / Q000188:drug therapy / Q000503:physiopathology; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000145:classification* / Q000188:drug therapy / Q000503:physiopathology*
chemical_list: D002121:Calcium Channel Blockers; D005456:Fluorescent Dyes; D011726:Pyridinium Compounds; D026941:Sodium Channel Blockers; D005711:Gallopamil; D013779:Tetrodotoxin; C050019:1-(3-sulfonatopropyl)-4-(beta)(2-(di-n-butylamino)-6-naphthylvinyl)pyridinium betaine