Correlation between tissue depolarizations and damage in focal ischemic rat brain

Ischemia-induced depolarizations may play a key role in the development of cerebral ischemic injury. Our goal was to assess the relationship between t issue depolarizations and tissue damage in focal ischemia. We performed mul ti-electrode cortical direct current (DC) potential recording and, subseque ntly, diffusion-weighted and T-2-weighted magnetic resonance imaging (MRI) in rats after i) cortical application of KCI, and ii) permanent and transie nt middle cerebral artery (MCA)-occlusion in rats. Cortical KCI application induced 10.0 +/- 2.2 transient negative DC potential shifts per h on the i psilateral hemisphere (i.e. cortical spreading depressions) (n = 4). During 6 h of permanent MCA-occlusion (n = 9) 1-10 DC potential shifts were obser ved, dependent on the brain location. Anoxic depolarization developed in th e ischemic core. Outside ischemic areas DC potential shifts resembled corti cal spreading depressions. Depolarizations in cortical ischemic borderzones were also transient, but generally long-lasting. Reperfusion induced 1 (n = 5) or 3 h (n = 6) after MCA-occlusion resulted in repolarization in 2.9 /- 1 5 min. Ischemic lesion volumes after 7 h, calculated from diffusion-we ighted and T-2-weighted MR images, correlated significantly with total depo larization time in cortical perifocal zones (R = 0.741, p < 0.05), but not with the number of depolarizations. The extent of ischemic damage, as measu red from alterations in the water diffusion coefficient and T-2, was also s ignificantly related to the total time of depolarization (R = 0.762 and 0.7 38, respectively, p < 0.01). We conclude that early ischemic tissue injury is related to the total duration of tissue depolarization and not to the fr equency of depolarizations. (C) 1999 Elsevier Science B.V. All rights reser ved.