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J Cereb Blood Flow Metab. 1996 Nov;16(6):1090-9.

Potassium-induced cortical spreading depressions during focal cerebral ischemia in rats: contribution to lesion growth assessed by diffusion-weighted NMR and biochemical imaging.

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Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, Cologne, FR Germany.


In focal ischemia of rats, the volume of ischemic lesion correlates with the number of peri-infarct depolarizations. To test the hypothesis that depolarizations accelerate infarct growth, we combined focal ischemia with externally evoked spreading depression (SD) waves. Ischemic brain infarcts were produced in halothane-anaesthetized rats by intraluminal thread occlusion of the middle cerebral artery (MCA). In one group of animals, repeated SDs were evoked at 15-min intervals by microinjections of potassium acetate into the frontal cortex. In another group, the spread of the potassium-evoked depolarizations was prevented by application of the N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine (MK-801). The volume of ischemic lesion was monitored for 2 h by diffusion-weighted imaging (DWI) and correlated with electro-physiological recordings and biochemical imaging techniques. In untreated rats, each microinjection produced an SD wave and a stepwise rise of the volume and signal intensity of the DWI-visible cortical lesion. The volume of this lesion increased between 15 min and 2 h of MCA occlusion from 19 +/- 15% to 66 +/- 16% of ipsilateral cortex. In dizocilpine-treated animals, microinjections of potassium did not evoke SDs, nor did the volume and signal intensity of the DWI-visible cortical lesion change. At 15 min after MCA occlusion, the DWI-visible lesion was larger than in untreated animals-43 +/- 16% of the ipsilateral cortex; however, after 2 h, it increased only slightly further to 49 +/- 21%. Slower lesion growth in the absence of SDs was also reflected by the volume of ATP-depleted tissue, which, after 2 h of MCA occlusion, involved 26 +/- 12% of the ipsilateral cortex in treated and 49 +/- 9% in untreated animals (p < 0.01). These observations support the hypothesis that peri-infarct depolarizations accelerate cerebral infarct growth.

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