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Adult male gerbils were submitted to 5-minute cerebral ischemia by bilateral carotid artery occlusion. At the end of ischemia and at various recirculation times ranging from 15 to 120 minutes, brains were frozen in situ and the regional distribution of ATP, glucose, and tissue pH was studied on coronal cryostat sections by bioluminescent and fluoroscopic techniques. During ischemia ATP was completely depleted, glucose decreased to< 10% of control, and regional tissue pH decreased from 7.04-7.09 to about 6.0. After the beginning of recirculation tissue pH and the regional content of metabolites exhibited a triphasic course. After 15 minutes pH returned to or even above normal, and ATP-and glucose-induced bioluminescence normalized. However, there was a secondary deterioration of both tissue acidosis and the metabolic state after 30 minutes. After longer recirculation times changes again improved and returned to normal within 2 hours. These changes were similar in all brain regions with the exception of the CA1 sector of the hippocampus, where the transient normalization of tissue pH was absent after 15 minutes of recirculation. This finding is in line with the previously observed microcirculatory insufficiency of this area and demonstrates that the CA1 sector of the hippocampus suffers more pronounced postischemic acidosis than other less vulnerable regions of the brain. (Stroke 1987;18:412-417)

Focal cerebral ischemia was produced in monkeys by injection of autologous clots into the left internal carotid artery. Regional protein synthesis was studied 2 hours after embolism by autoradiographic and biochemical evaluation of [ 1 H]phenylaIanine incorporation into brain proteins, and the results were correlated with electrophysiologic (electroencephalogram, evoked potentials) and light microscopic observations. Ischemic territories were clearly identified on autoradiograms as sharply demarcated areas with reduced radioactivity. The localization of regions with reduced protein biosynthesis correlated with the early postembolic suppression of evoked potentials but not with the (improved) functional state and the morphologic alterations at the end of the experiment. Suppression of amino add incorporation, in consequence, is a long-lasting event that allows documentation of the initial embolic impact for at least 2 hours irrespective of the subsequent recovery process. (Stroke

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