[K+]o accumulation and electrophysiological alterations during early myocardial ischemia.
Double-barreled valinomycin K+-sensitive electrodes and floating microelectrodes were used to monitor extracellular K+ concentration ([K+]o) and intracellular potential, respectively, in the isolated arterially perfused rabbit interventricular septum, under conditions of global ischemia without collateral flow and hypoxia with maintained flow. During ischemia [K+]o reproducibly increased at rates of 0.5-1 mM/min, usually in a triphasic pattern, and was accompanied by shortening of the action potential duration (APD) and an increase in conduction time (CT). Hyperkalemia, equivalent to that occurring during ischemia, in combination with respiratory acidosis (pH 6.2-6.5) and catecholamines reproduced quantitatively the ischemia-induced changes in APD and CT. None of these factors alone produced quantitatively comparable electrophysiological changes. Faster heart rates increased [K+]o accumulation during ischemia and accentuated the changes in APD and CT during ischemia. These findings suggest that local hyperkalemia, intracellular acidosis, and catecholamines release during early ischemia may account for electrophysiological changes predisposing to the development of reentrant arrhythmias.
D000142:Acidosis, Respiratory / Q000503:physiopathology; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D003327:Coronary Disease / Q000378:metabolism* / Q000503:physiopathology; D004553:Electric Conductivity; D004594:Electrophysiology; D004837:Epinephrine / Q000494:pharmacology; D005110:Extracellular Space / Q000378:metabolism; D005947:Glucose / Q000494:pharmacology; D006947:Hyperkalemia / Q000503:physiopathology; D009638:Norepinephrine / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D011817:Rabbits; D013997:Time Factors
D005947:Glucose; D011188:Potassium; D009638:Norepinephrine; D004837:Epinephrine