Neuroscience Research Institute, University of Ottawa, Ottawa, Ontario, Canada

Correspondence: Antoine M Hakim, Neuroscience Research Institute, University of Ottawa, 451 Smyth Road, Ottawa, Ontario, KIH 8M5, Canada.

Received 10 February 1995; Revised 14 July 1995; Accepted 18 July 1995.

Abstract

The possibility that cortical spreading depression (CSD) may have neuroprotective action during subsequent focal cerebral ischemia was examined in rats. Three days before the imposition of focal cerebral ischemia CSDs were elicited by applying potassium chloride (KCl) for 2 h through a microdialysis probe implanted in the occipital cortex. Control animals were handled identically except that saline was infused instead of KCl. Focal ischemia was produced by the intraluminal suture method and cortical and subcortical infarct volumes were measured 7 days later. Neocortical infarct volume was reduced from 124.8 49.5 mm³ in the controls to 62.9 59.5 mm³ in the animals preconditioned with CSD (p = 0.012). There was no difference between the two groups in the subcortical infarct volume or in CBF, measured by the hydrogen clearance method, during or immediately after the ischemic interval. Our data indicate that preconditioning CSD applied 3 days before middle cerebral artery occlusion may increase the brain's resistance to focal ischemic damage and may be used as a model to explore the neuroprotective molecular responses of neuronal and glial cells.