A newly developed model of transient global ischemia in the rat was evaluated by magnetic resonance imaging (MRI) in terms of localization of brain lesions, their extent and severity, and temporal evolution. Such a model, consisting of bilateral occlusion of common carotid arteries for 10 minutes and mild hypoxia (15% O2) for 20 minutes induces delayed neuronal degeneration, necrosis, and gliosis (detected histologically and immunohistochemically). Ischemia was assessed by full suppression of spontaneous electroencephalographic activity. A "hybrid" T2-/diffusion-weighted MR sequence enhancing more effectively the contrast between injured and intact tissues as compared to T2-weighted MRI was used at 24, 48, 72, and 96 hours and at 7 days postischemia. Twenty hypoxic-ischemic rats showed a considerable variability in brain damage. In 8, there were no MRI-detectable lesions at any interval. In the other 12 rats, the severity and extension of neuronal damage varied markedly, but the lesions were always localized (monolaterally in 8 and bilaterally in 4 rats) in the occipital, temporal, or parietal cerebral cortex. Mainly, they were of intermediate severity or were severe (as assessed by MRI hyperintensity) and were accompanied by usually less severe lesions in the thalamus and/or caudate putamen. The hippocampus was affected moderately or severely in 4 of 12 rats. In most cases, there was at 48 hours a considerable growth in severity and/or extension of lesions, which usually remained stable at later intervals. In conclusion, MRI allowed us to follow brain lesions during the first week in this relatively simple and noninvasive model of transient global ischemia.