title: Differential role of epicardial and endocardial K(ATP) channels in potassium accumulation during regional ischemia induced by embolization of a coronary artery with latex.
abstract: BACKGROUND
  K(ATP) channels are activated predominantly in the epicardium during regional ischemia. Therefore, the role of K(ATP) channels in ischemia-induced rise of extracellular potassium concentration ([K+]o) might be greater in the epicardium.
  
  
  RESULTS
  In 18 anesthetized dogs, the left anterior descending coronary artery (LAD) was ligated, followed by injection of 23-microm latex beads into the occluded artery to interrupt collateral flow, by which accumulated [K+]o might wash out. Epicardial and endocardial [K+]o were measured during a 20-minute period of ischemia using a valinomycin membrane. The dogs were divided into three groups: 6 control dogs (CTRL); 7 dogs pretreated with intravenous glibenclamide (0.3 mg/kg [GLIB]), a blocker of K(ATP) channels; and 5 dogs pretreated with intravenous nicorandil (0.2 to 0.25 mg/kg [NCR]), a K(ATP) channel opener. Before LAD occlusion, there was no difference in [K+]o among the three groups. In the control group, epicardial and endocardial [K+]o were increased to a similar level as a function of time after occlusion (CTRL) at both layers. Ischemia-induced epicardial [K+]o rise was suppressed by GLIB (8.4+/-0.4 vs 6.7+/-0.5 mM, P < 0.05) but augmented by NCR (12.9+/-2.0 mM, P < 0.05). In contrast, endocardial [K+]o rise remained unaffected (7.6+/-0.2 mM CTRL, 7.6+/-1.3 mM GLIB, and 9.4+/-2.2 mM NCR, P = NS).
  
  
  CONCLUSIONS
  Activation of K(ATP) channels plays an important role in epicardial [K+]o rise, but not in endocardial [K+]o rise, during regional ischemia. Another mechanism(s) may be important for endocardial [K+]o accumulation.
authors.affiliation: Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan. smiyoshi@cpnet.med.keio.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Miyoshi
authors.forename: T
authors.initials: T
authors.lastname: Miyazaki
authors.forename: M
authors.initials: M
authors.lastname: Asanagi
authors.forename: K
authors.initials: K
authors.lastname: Moritani
authors.forename: S
authors.initials: S
authors.lastname: Ogawa
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D000465:Algorithms; D000818:Animals; D003331:Coronary Vessels / Q000502:physiology*; D004285:Dogs; D004621:Embolization, Therapeutic; D004699:Endocardium / Q000187:drug effects / Q000378:metabolism*; D005905:Glyburide / Q000494:pharmacology; D008839:Microelectrodes; D008863:Microspheres; D017202:Myocardial Ischemia / Q000378:metabolism*; D009536:Niacinamide / Q000031:analogs & derivatives / Q000494:pharmacology; D020108:Nicorandil; D010496:Pericardium / Q000187:drug effects / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000819:agonists / Q000378:metabolism*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D026902:Potassium Channel Blockers; D015221:Potassium Channels; D014665:Vasodilator Agents; D009536:Niacinamide; D020108:Nicorandil; D000255:Adenosine Triphosphate; D011188:Potassium; D005905:Glyburide