title: Rapid inward current in ischemically-injured subepicardial myocytes bordering myocardial infarction.
abstract: BACKGROUND
  To determine if collagenase-dispersed epicardial myocytes overlying myocardial infarction reproduce the same altered electrophysiology observed in intact epicardium, multicellular tissue preparations and enzymatically-dispersed myocytes from ischemically-injured canine subepicardium were examined 1 and 4 days after myocardial infarction.
  
  
  RESULTS
  The electrophysiologic changes observed with ischemic injury in enzymatically-dispersed myocytes were not different from changes observed in multicellular tissue preparations at 1 and 4 days postinfarction. Ischemically-injured myocytes were depolarized versus normal myocytes at [K0]+ (2.5 to 40 mM) with reduced membrane potentials also observed in injured subepicardial tissue preparations [K0]+ (4 to 24 mM). On day 1, the reduced Vmax and the prolonged recovery of Vmax from inactivation were consistent with the reduced membrane potentials observed at each [K0]+. The half-maximal Vmax, maximal Vmax, and Boltzmann constant (k) in injured myocytes were unchanged versus normal myocytes. On day 4 postinfarction, the half-maximal Vmax was shifted to a more negative membrane potential, the maximal Vmax was reduced, and k was increased in injured versus normal myocytes. Prolonged recovery from inactivation was observed with depressed membrane potentials in injured myocytes on day 4.
  
  
  CONCLUSIONS
  Enzymatically-dispersed myocytes from ischemically-injured subepicardium closely reproduce altered cellular properties observed in multicellular tissue preparations. The data suggest that 1 day postinfarction, altered conduction and refractoriness largely result from a reduced membrane potential. At 4 days, a reduced maximal Vmax, a shift in the inactivation curve to more negative voltages, and prolonged recovery of Vmax from inactivation also contribute to slowed conduction and prolonged refractoriness.
authors.affiliation: Department of Pharmacology, University of Oklahoma Health Sciences Center, Oklahoma City.
authors.forename: E
authors.initials: E
authors.lastname: Patterson
authors.forename: B J
authors.initials: BJ
authors.lastname: Scherlag
authors.forename: R
authors.initials: R
authors.lastname: Lazzara
mesh_terms: D000818:Animals; D001158:Arteries / Q000473:pathology / Q000503:physiopathology; D002463:Cell Membrane Permeability / Q000502:physiology; D002469:Cell Separation; D003327:Coronary Disease / Q000473:pathology / Q000503:physiopathology; D003331:Coronary Vessels / Q000473:pathology / Q000503:physiopathology; D004285:Dogs; D004558:Electric Stimulation; D006329:Heart Conduction System / Q000502:physiology; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D009203:Myocardial Infarction / Q000473:pathology* / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000473:pathology* / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology* / Q000648:ultrastructure; D013997:Time Factors