Abstract A three- to fourfold increase in brain lactate was observed in rats and dogs 6 min after circulatory arrest. This did not change significantly during the following 84 min of observation. Carotid artery perfusion with 37 and 0 C isotonic saline altered this rise slightly, while perfusion with 24 C saline did not. Addition of 6.67 mmole/liter glucose to the perfusate caused a significantly higher rise in brain lactate at 37, but not at 0 C. These experiments are in agreement with evidence from reports of others which suggest that the glycolytic pathway is preserved in anoxic, hypothermic brain, but not in anoxic, normothermic brain. When compared with previous survivial experiments, they indicate that cerebral lactic acid cannot be used as an index of brain viability.