Cerebral energy metabolism during recovery from carbon monoxide hypoxia-oligemia.

The effects of 1 h exposure to 1% CO and right common carotid artery clamping upon the cerebral energy metabolism, perfusion and histology were studied in anesthetized (70%N(2)O) and unanesthetized rats following reoxygenation for 0-6 h. At 0 h recovery the clamped hemispheres showed decreases of ATP, PCr and glycogen, and increases of ADP, AMP, inorganic phosphate and lactate which indicated an advanced derangement of the tissues' energy homeostasis. Exposure in unanesthetized animals was associated with lower levels of ATP and glycogen, and with larger increases of lactate in the clamped hemisphere which suggested the presence of a more intense hypoxic-oligemic insult. The metabolic differences in the clamped hemisphere of unanesthetized and anesthetized animals became more marked after 1 h reoxygenation, with anesthetized animals showing large restitutions of ATP, PCr, glycogen and lactate, whereas in unanesthetized animals these metabolites showed severe persistent defects over the 6 h reoxygenation period. Since the arterial oxygen content and tension, and perfusion patterns were equivalent in the 2 series at 0 and 1 h recovery, it is concluded that even minor anesthetic agents such as 70%N(2)O or other non-hypoxic variables during exposure or recovery may cause significant alterations in the metabolic restitution of the hypoxic-oligemic brain.