Thirty-two pairs (n = 64) of Mongolian gerbils were surface cooled to 18 degrees C and randomly subjected to 0 to 180 minutes of bilateral carotid occlusion in the neck. They were rewarmed after release of the carotid occlusion. After rewarming, one member of each pair was allowed to survive 7 days and then was put to death for brain histologic study; the other was subjected to brain preservation by quick freezing for subsequent biochemical studies. In the survivors, neurologic function was depressed during the 7 subsequent days, and the depression was in direct relation to the time of carotid occlusion (p = 0.0005). The proportion of normal hippocampal neurons decreased in direct proportion to the length of carotid occlusion (p less than 0.0001). The depression in neurologic function and in the proportion of normal neurons was evident when occlusion time exceeded 45 minutes. The proportion of normal neurons was correlated with neurologic function (r = 0.56, p = 0.0001). Cortical adenosine triphosphate (ATP) concentration after brain reperfusion was reduced in comparison with normal and varied inversely with carotid occlusion time (r = -0.84, p less than 0.0001). Alanine (p less than 0.001), lactate (p = 0.01), and pyruvate (p = 0.001) concentrations were elevated, in direct relation to carotid occlusion time. These observations are consistent with other experimental studies of profoundly hypothermic total circulatory arrest and indicate the damaging effect of this modality, particularly when the circulatory arrest time exceeds 45 minutes.