1. ¹Department of Bioengineering, Imperial College, London, UK
2. ²Department of Clinical Neuroscience, King's College London, London, UK
3. ³Max Planck Institute for Neurological Research, Köln, Germany
4. ⁴Department of Neurology and Experimental Neurology, Charité University of Medicine, Berlin, Germany

Correspondence: Dr P Hashemi, Department of Chemistry, The University of North Carolina at Chapel Hill, B-5 Venable Hall, Chapel Hill, NC 27599, USA. E-mail: phashemi@email.unc.edu

Received 12 February 2008; Revised 12 July 2008; Accepted 11 August 2008; Published online 24 September 2008.

Abstract

Rapid sampling microdialysis (rsMD) directed towards the cerebral cortex has allowed identification of a combined time-series signature for glucose and lactate that characterizes peri-infarct depolarization in experimental focal ischaemia, but no comparable data exist for 'classical' cortical spreading depression (CSD) associated with hyperaemia in the normally perfused brain. Here, we examined the rsMD responses of dialysate glucose and lactate to five hyperaemic spreading depressions induced with intracortical microinjections, typically of 1 mol/L KCl, in open-skull preparations in five cats under chloralose anaesthesia. Depolarization was verified with microelectrodes, and laser speckle flowmetry was used to examine propagation of the events and perfusion responses near the MD probe. Ten minutes after depolarization, dialysate glucose fell and lactate rose by 28% and 58% respectively. There was no recovery of dialysate glucose 30 mins after depolarization. Mean baseline indicative cerebral blood flow was 25.54.1 mL/100 g/min and mean maximum hyperaemic increase was by 29.66 mL/100 g/min; hyperaemia remained present 30 mins after CSD. As CSD events are repetitive, frequent, and often clustered temporally in human acute brain injury, these results indicate a high risk of depletion of extracellular glucose in association with depolarization events of a pattern previously thought to be largely benign.