Failure of microvascular re-perfusion, no reflow, of the brain after a period of ischemia has been proposed as the etiology of the cerebral dysfunction frequently seen in patients after resuscitation from hemorrhagic shock. For this investigation rats were stressed by subjecting them to a period of combined hypoxia and hypotension followed by resuscitation. Micro-oxygen electrodes measured brain oxygen tension, thus allowing an assessment of the distribution of cerebral blood flow, during stress and after resuscitation. After resuscitation, a hyperemic response was noted, followed by gradual return of some areas of the brain to normal perfusion, while other areas remained hyperemic for at least 2 hours post-resuscitation. On the basis of these results there appears to be no support for the no-reflow hypothesis. These data imply that therapeutic modalities aimed at increasing cerebral blood flow and oxygenation in the post-resuscitation period are insufficient in themselves for improved survival of patients sustaining a hypotensive, hypoxic episode.