Extracellular K+ and H+ shifts in early ischemia: mechanisms and relation to changes in impulse propagation.
Heart and skeletal muscle cells rapidly lose potassium ions after withdrawal of oxygen. In myocardial ischemia, cellular release of potassium and interruption of extracellular washout produce a rapid and marked increase of extracellular K+ concentration. Harris et al. were the first to observe the coincidence of the K+ shift and the frequent occurrence of ventricular arrhythmias. They ascribed a major role to K+ in the genesis of the electrophysiological changes in early ischemia. The purpose of this article is to outline briefly in the first part the relationship between potassium accumulation and the electrical changes in ischemia with emphasis on reviewing the role of K+ in the slowing of impulse propagation and production of conduction block. In the second part, the possible mechanisms leading to potassium imbalance will be discussed and experimental data will be presented which suggest that an important component of net potassium loss is related to the development of acidosis.
D000138:Acidosis / Q000378:metabolism; D000818:Animals; D003327:Coronary Disease / Q000378:metabolism* / Q000503:physiopathology; D005110:Extracellular Space / Q000378:metabolism; D006168:Guinea Pigs; D006329:Heart Conduction System / Q000503:physiopathology*; D006863:Hydrogen-Ion Concentration; D007473:Ion Channels / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*
D007473:Ion Channels; D011188:Potassium