Abstract In an effort to elucidate the mechanism by which parts of the human CNS, once deprived of oxygen and/or nutritive supply, remain susceptible to another episode of oxygen deprivation, young adult Sprague-Dawley rats were exposed to several forms of hypoxia. Unilateral and bilateral carotid ligations were performed on some, others were placed in a hypoxic atmosphere 1–6 days following unilateral carotid ligation and others were exposed to the hypoxic atmosphere only. The brains of all rats were examined histochemically for changes in glycogen and its related enzymes and in oxidoreductive enzymic activity. Typical lesions with appropriate changes in related glycogen and enzymic reaction were seen in the hypoxic, ischaemichypoxic and sometimes in the bilateral ischaemic brains. The unilateral ischaemic brains underwent only a transient reduction in phosphorylase activity and glycogen content and yet remained susceptible to hypoxia up to 6 days later. Reasons for this residual susceptibility, especially in certain “sensitive” areas, and the possible reasons for the “sensitivity” of these areas in the first place are discussed, especially in relation to the findings in the other models.