Cortical Negative DC Deflections following Middle Cerebral Artery Occlusion and KCl-Induced Spreading Depression: Effect on Blood Flow, Tissue Oxygenation, and Electroencephalogram

Abstract

In the periphery of ischemic brain lesions, transient spreading depression-like direct current (DC) deflections occur that may be of pathophysiological importance for determining the volume of the ischemic infarct. The effect of these deflections on cerebral blood flow, tissue oxygen tension, and electrophysiology was studied in rats submitted to intraluminal thread occlusion of the middle cerebral artery (MCA) and compared with the changes following potassium chloride (KCl)-induced spreading depression of intact animals. Immediately after MCA occlusion, cortical laser–Doppler flow (LDF) in the periphery of the MCA territory sharply decreased to 35 ± 14% of control (mean ± SD; p < 0.05), tissue Po2 declined from 28 ± 4 to 21 ± 3 mm Hg (p < 0.05), and EEG power fell to ∼80% of control. During 7-h occlusion, 3–11 DC deflections with a mean duration of 5.2 ± 4.8 min occurred at irregular intervals, and EEG power gradually declined to 66 ± 16% of control (p < 0.05). During the passage of DC deflections, LDF did not change, but Po2 further declined to 19 ± 4 mm Hg (p < 0.05). KCl-induced depolarizations of intact rats were significantly shorter (1.4 ± 0.5 min; p < 0.05) and were accompanied by a 43% increase in LDF (p < 0.05) and a slight but significant increase in tissue Po2 from 22 ± 4 to 25 ± 4 mm Hg (p < 0.05). The comparison of periinfarct and KCl-induced depolarizations demonstrates that oxygen requirements are not coupled to an appropriate flow response in the periinfarct zone with severely reduced blood flow. The resulting episodes of relative hypoxia could explain the previously documented relationship between the number of depolarizations and infarct volume.