Previous studies have established that in cerebral cortex subjected to progressive reduction in blood flow, two distinct thresholds of flow may be identified below which cellular function is impaired: the cortical evoked response loses amplitude when local flow falls below 18ml/100gm/min, and below 11ml/100gm/min a major increase in extracellular K+ activity (Ke) occurs. However, further evidence suggests that even at higher flows the capacity of the tissue to handle induced ionic changes may be impaired. To investigate this point, we studied the kinetics of resolution of Ke following a transient increase produced by local electrical stimulation, in relation to the local pre-stimulus flow (reduced by acute middle cerebral artery occlusion) in baboons. Flow was measured by the hydrogen clearance method and Ke by ion-exchanger micro-electrodes, in the same cortical regions. In primary induced transients (those increases in Ke elicited by cortical stimulation, and reported previously,) Ke attained a maximum value of 8-10 mM and then decayed towards the 4-mM baseline. The half-time of this decay was significantly increased from normal in the flow range 20–40 ml/100gm/min, and increased further at lower flows until, below 11ml/100gm/min, Ke clearance was undetectable. Thus, cortical ion homeostasis appeared impaired at flows substantially closer to normal than those thresholds mentioned above, a result discussed in terms of impairment of active Ke clearance mechanisms. Secondary induced transients arose during a primary induced transient, reaching considerably higher peak values (8–30 mM) of Ke (indicating temporary clearance loss) and with slower decay rate than the primary. Spontaneous transients, not associated with any stimulus, were also observed; like secondary transients, they occurred only at flows below 20ml/100gm/min and showed a reduction in clearance rate with progressive ischemia. They resemble spreading depression and their generation is discussed in terms of the ionic and metabolic conditions at their time of origin.