Ischemic brain lesions were induced in adult Wistar and Fischer rats by temporary occlusion of the bilateral common carotid artery. The severity of ischemic lesions depended on the duration of carotid occlusion. While 2 h occlusion resulted in 15 deaths among 40 rats and the development of ischemic lesions in 16 of 25 asymptomatic survivors, none died after 0.5 h occlusion and yet 13 of 30 apparently asymptomatic rats had ischemic lesions when examined on day 7. Histological examination combined with immunohistochemistry of autologous albumin for assessing the integrity of the blood-brain barrier (BBB) revealed two distinct lesions: (1) ischemic neural damage with extensive tissue permeation of serum albumin, (2) death of individual neurons sparing other neural elements in the absence of the BBB breakdown. Ischemic neural damage with BBB breakdown was common in animals dying within 48 h after reflow. The lesions without BBB breakdown, on the other hand, were found solely in asymptomatic animals in which groups of severely degenerated neurons were preferentially located in the CA 1 region of the hippocampus, the caudoputamen and deeper layers of the neocortex. The sequential measurements of regional cerebral blood flow (rCBF) in the bilateral hippocampus by the hydrogen clearance method disclosed a steady decrease in rCBF after the occlusion, 51% of the pre-occlusion state at 10 min, 35% at 25 min and 32% at 40 min. The simplicity of procedure could make this model suitable for the study of the pathogenesis of ischemic neuronal damage in a critically low perfusion state.