The Impact of Extracellular Potassium Accumulation in Stroke

The involvement of the potassium ion and its movements in stroke is reviewed. There are two potassium pools which do not mix easily: serum potassium, which is subject to dietary fluctuations and potassium in the parenchyma, which is protected from outside fluctuations by the blood–brain barrier, but is subject to internal shifts driven by neuronal activity. Dietary increase in potassium is reducing stroke risk probably due to action on radical oxygen species. The blood–brain barrier has a very low permeability to potassium and this does not change in stroke. In the case brain edema develops there is solute transfer driven by the bumetanide-sensitive 2Na-K-Cl carrier in endothelial cells. In the parenchyma, extracellular potassium exhibits massive shifts which are indicative of the health of the ischemic tissue, especially in focal stroke. Spreading depression waves develop in focal ischemia with potassium shifts the main indicator. Spreading depression is a double-edged sword: it damages the penumbra irreversibly. In healthy tissue it has a beneficial effect and leads to pre-ischemic conditioning. This phenomenon is based on the protective effect of reactive astrocytes on ailing neurons in the first phase after injury.