CORTICAL NEGATIVE DC DEFLECTIONS FOLLOWING MIDDLE CEREBRAL-ARTERY OCCLUSION AND KCL-INDUCED SPREADING DEPRESSION - EFFECT ON BLOOD-FLOW, TISSUE OXYGENATION, AND ELECTROENCEPHALOGRAM

In the periphery of ischemic brain lesions, transient spreading depres sion-like direct current (DC) deflections occur that may be of pathoph ysiological importance for determining the volume of the ischemic infa rct. The effect of these deflections on cerebral blood flow, tissue ox ygen tension, and electrophysiology was studied in rats submitted to i ntraluminal thread occlusion of the middle cerebral artery (MCA) and c ompared with the changes following potassium chloride (KCl)-induced sp reading depression of intact animals. Immediately after MCA occlusion, cortical laser-Doppler flow (LDF) in the periphery of the MCA territo ry 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 similar to 80% of control. During 7-h occlusion, 3-1 1 DC deflections with a mean duration of 5.2 +/- 4.8 min occurred at i rregular 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-ind uced 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 K Cl-induced depolarizations demonstrates that oxygen requirements are n ot coupled to an appropriate flow response in the periinfarct zone wit h severely reduced blood flow. The resulting episodes of relative hypo xia could explain the previously documented relationship between the n umber of depolarizations and infarct volume.