Extracellular K+ activity (Ke), local tissue blood flow and the cortical evoked potential (EP) were measured concurrently in the cerebral cortex of baboons anaesthetised with a-chloralose. Flows were progressively reduced from normal by occlusion of the middle cerebral artery and controlled steps of exsanguination. Our data suggest that 3 stages may be identified in the disturbance of K+ homeostasis produced by progressive ischaemia. In the first stage, at flow levels similar to those sufficient to abolish the EP (12-16 ml/100 g/min), small, self-limiting increases in Ke occur, probably reflecting K+ efflux into the extracellular space (ECS) with partial impairment of K+ clearance from the ECS. The second stage occurs at distinctly lower (P less than 0.01) levels of flow (8-11 ml/100 g/min), and is characterized by a massive (30-80 mM) increase in Ke, which we attribute to an increase in ionic permeability of cell membranes with further impairment or overloading of K+ clearance mechanisms. In the third stage, at flows below about 6-8 ml/100 g/min, the data indicate an inverse relationship between flow and Ke with persisting high Ke levels, suggesting complete loss of K+ clearance. Transient increases of Ke also occur in the flow range 4-13 ml/100 g/min, the rate of recovery of Ke in their decay phase being positively corelated with flow (P less than 0.005).