Factors influencing survival of neurons during ischemia and neuronal revival after ischemia are reviewed. During ischemia, biochemical and electro-physiological changes depend on residual blood flow rate: below 30 to 40 ml/100 g/min EEG amplitude decreases, below 18 ml/100 g/min spontaneous neuronal activity ceases, and below 10 ml/100 g/min cell membranes depolarize. Attempts to improve blood flow after middle cerebral artery occlusion with vasoactive drugs were not successful but there was an indication that the calcium antagonist nimodipine reduced ischemia-induced disturbances of ion homeostasis. Revival after ischemia depends mainly on post-ischemic hemodynamic factors, such as the no-reflow phenomenon or delayed post-ischemic hypoperfusion. No-reflow was successfully treated by induced hypertension, anticoagulation, and osmotherapy. Delayed post-ischemic hypoperfusion and the associated metabolic disturbances could not be ameliorated by either vasoactive drugs including prostacyclin, nor by metabolic inhibition with barbiturates and hypothermia. The disturbance of metabolic regulation of blood flow during post-ischemic hypoperfusion, therefore, remains one of the main problems of post-ischemic resuscitation.