The hypothesis that lactate and free fatty acids (FFA) are elevated in the first minutes after subarachnoid hemorrhage (SAH) is tested. Adult rats were subjected to an endovascular SAH through the right internal carotid artery while under anesthesia. The brains were frozen in-situ at 15, 30, 60 min, and 24 h post-hemorrhage. Regional measures of tissue lactic acid and FFA were made in the hippocampi, ipsilateral cortex, contralateral cortex, and cerebellum. Lactic acid levels were significantly elevated from sham animals in each region within the first hour (p<0.0001 cerebellum, right, and contralateral cortex, p<0.01 hippocampus), but did not change significantly over the first hour. At 24 h post-hemorrhage, there was no significant difference in the lactic acid levels from controls. Similarly, total FFA were significantly higher in each region as compared to sham operated controls within the first hour (p<0.001 cerebellum, p<0.05 hippocampus, p<0.05 contralateral cortex, p<0.0001 ipsilateral cortex). By 24 h, there was no significant difference in FFA levels from shams. The data indicate that aerobic metabolism fails and cellular damage with degradation of cell membranes occurs in the first minutes after SAH, and lasts for at least 1 h. However, this process is stabilized within 24 h in our model. Although the largest effect was seen in the ipsilateral cortex, all areas of the brain were effected.