Cation activities in reversible ischemia of the cat brain.

In normothermic anesthetized cats cerebral blood flow was interrupted completely for one hour by arterial clamping and induced hypotension. The effect of ischemia on the ionic gradients of the cerebral cortex was assayed by determining total cortical electrolytes and by recording the activities of extracellular potassium (K+i1e) and subarachnoid sodium ions ([Na+)s) with ion-sensitive electrodes. During ischemia K+e increased from 3.3+/-0.3 to 56+/-5.4 mEq per liter (means+/-SE) and Na+s decreased from 133+/-3.8 to 53+/-5.8 mEq per liter. When the brains were recirculated with blood after one hour's ischemia, K+e and Na+a gradually returned to normal within 45 minutes. The calculated intracellular uptake of sodium during ischemia amounted to 139 mEq per kilogram dry weight, whereas the intracellular release of potassium was only 64 mEq per kilogram. The increase in intracellular cation was accompanied by a movement of water from the extracellular into the intracellular compartment, causing a reversible shrinkage of the extracellular space from 18.9 to 8.5 vol %. The changes in ionic gradients were related to the development and resolution of ischemic brain swelling, and to the elctrophysiological events during and after ischemia.