INTRODUCTION: 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. METHODS AND 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). CONCLUSION: 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.
INTRODUCTION: 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. METHODS AND 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). CONCLUSION: 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: Tyson G Taylor; Paul W Venable; Junko Shibayama; Mark Warren; Alexey V Zaitsev Journal: Am J Physiol Heart Circ Physiol Date: 2012-03-30 Impact factor: 4.733