Using the canine thalamic infarction model, hemodynamics, CO2 responses and thalamic EEG changes were studied in 7 dogs. Of the 7 animals, 4 showed hemorrhagic infarction and 3 did not, following recirculation after 6 hours of vascular occlusion. 1) The rCBF threshold for producing hemorrhagic infarction when recirculation following 6 hours of vascular occlusion was approximately 50% of the pre-occlusion level. 2) rCBF of the animals showing hemorrhagic infarction included hyperperfusion due to recirculation, and then fell to a level below the pre-occlusion level in a relatively short period. The CO2 response became disturbed both during occlusion and after release of occlusion. Thalamic EEG was nearly flat during vascular occlusion and recovery was not seen following recirculation. 3) rCBF of the animals not showing hemorrhagic infarction recovered rapidly to the pre-occlusion level due to recirculation. The CO2 response was somewhat disturbed during occlusion, but recovered following recirculation. Thalamic EEG was well preserved both during occlusion and after release.