¹Department of Clinical Neurosciences, Section of Neurosurgery, King's College, London, UK

Correspondence: AJ Strong, Department of Neurosurgery, King's College, London SE5 9RS, UK. E-mail: anthony.strong@kcl.ac.uk

Received 19 July 2004; Accepted 14 September 2004; Published online 16 February 2005.

Abstract

Peri-infarct depolarisations (PIDs) contribute to infarct expansion in experimental focal ischaemia; furthermore, depolarisations propagate in the injured human brain. Glucose utilisation is increased under both conditions, and depletion of brain glucose carries a poor prognosis. We studied dynamics of cerebral glucose and lactate in relation to PID patterns in experimental stroke. The middle cerebral artery was occluded for 3 h in 23 cats under terminal chloralose anaesthesia. We used fluorescence imaging to detect occurrence of PIDs, and rapid-sampling online microdialysis (rsMD), coupled to a flow-injection assay, to examine changes in cerebral cortical extracellular glucose and lactate at intervals of 30 sec each. After 30 min' ischaemia, lactate had increased by 43.6s.d. 45.9 mol/L, and stabilised in that range for 3 h. In contrast, glucose fell only slightly initially (11.99.7 mol/L), but progressively decreased to a reduction of 56.747.2 mol/L at 3 h, with no evidence of stabilisation. There was a highly significant inverse relationship of frequency of PIDs with plasma glucose (P<0.001). The results also characterise a metabolic signature for PIDs for possible application in clinical work, and emphasise potential risks in the use of insulin to control plasma glucose in patients with brain injury.