title: Differences in the effect of metabolic inhibition on action potentials and calcium currents in endocardial and epicardial cells.
abstract: BACKGROUND
  Ischemia-induced electrophysiological changes are more prominent in epicardial cells than in endocardial cells. Epicardial action potentials shorten more than endocardial action potentials during ischemia. Since the L-type Ca2+ current plays an important role in the maintenance of action potential duration, we hypothesized that the Ca2+ current is affected more in epicardial cells than in endocardial cells during ischemia.
  
  
  RESULTS
  To test this hypothesis, we examined the effect of metabolic inhibition, a major component of ischemia, on action potentials and the Ca2+ current in single cells isolated from the endocardial and epicardial layers of the feline left ventricle. The membrane voltage and current were measured by using the whole-cell mode of the patch-clamp technique. During control periods, action potentials recorded from epicardial myocytes had lower amplitude, a prominent notch between phases 1 and 2, and shorter action potential duration compared with those recorded from endocardial myocytes. However, the amplitude and current-voltage relation of the Ca2+ current were similar in endocardial and epicardial cells at test potentials of -30 to 60 mV elicited from a holding potential of -40 mV. The time course of inactivation of the Ca2+ current also was identical in the two cell types. After 15 minutes of superfusion with glucose-free Tyrode's solution containing 1 mM CN-, action potential duration was reduced by 13 +/- 7% in endocardial cells and by 80 +/- 9% in epicardial cells (p less than 0.01). The peak Ca2+ current was reduced by 21 +/- 9% in endocardial cells and by 37 +/- 6% in epicardial cells (p less than 0.01).
  
  
  CONCLUSIONS
  We conclude that enhanced depression of the Ca2+ current may account in part for the greater action potential shortening in epicardial cells during ischemia and metabolic inhibition.
authors.affiliation: Department of Medicine (Cardiology), University of Miami School of Medicine, FL 33101.
authors.forename: S
authors.initials: S
authors.lastname: Kimura
authors.forename: A L
authors.initials: AL
authors.lastname: Bassett
authors.forename: T
authors.initials: T
authors.lastname: Furukawa
authors.forename: N
authors.initials: N
authors.lastname: Furukawa
authors.forename: R J
authors.initials: RJ
authors.lastname: Myerburg
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000502:physiology*; D002415:Cats; D003486:Cyanides / Q000494:pharmacology; D004594:Electrophysiology; D004699:Endocardium / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D005260:Female; D008297:Male; D010496:Pericardium / Q000166:cytology / Q000378:metabolism / Q000502:physiology*
chemical_list: D003486:Cyanides; D002118:Calcium