E. Carmeliet, J. Vereecke
Journal name not available for this finding
Among the early changes in ion concentration during myocardial ischemia the rise in extracellular K+ concentration is the most pronounced. Four possible mechanisms are proposed and evaluated. They are not mutually exclusive and all probably play a role to a variable extent, depending on the degree of hypoxia versus ischemia: 1) Volume contraction of the extracellular space, secondary to the production of intracellular osmotically active molecules, can maximally explain a doubling of the normal K+ concentration. 2) Experimental evidence for inhibition of the active K+ inward transport is controversial. 3) No direct evidence exists for electroneutral K+ transport as a cotransport with anions or an exchange with cations. 4) An increase in electrogenic K+ outward movement has been demonstrated to occur in hypoxia and metabolic inhibition. As to the nature of the K+ current it is difficult to select one of the multiple K+ currents available. An increase in inward current is the conditio sine qua non to explain an important K+ loss at rest. The best candidates for K+ loss in stimulated preparations are the ATP-dependent, the Nai-activated, and the AA-activated K+ channels; they are time-independent and show outward rectification.