In rats with unilateral carotid artery ligation pyramidal tract responses were studied during hypoxia and during trimethaphan-induced hypotension. Observations on EEG activity during hypoxia suggest that unilateral carotid artery ligation produces a more severe perfusion defect in lateral portions of the hemisphere. During hypoxia and during trimethaphan-induced hypotension indirect PTRs disappeared first from the hemisphere on the side of carotid artery ligation and next from the opposite hemisphere. This was followed by loss of direct PTRs in the same order. Animals could not be resuscitated once the direct PTR from the non-ligated hemisphere had disappeared. Hypotension appears to be a late contributing factor in impairing electrocerebral activity during hypoxia in this study.