We have developed a model of haemodynamic cerebral ischaemia by inducing haemorrhagic hypotension (40-50 mmHg mean blood pressure) following unilateral common carotid occlusion, with external carotid ligation, in anaesthetised rats. The neuropathological pattern of ischaemic brain damage was correlated with the distribution of change in cerebral blood flow using the 14C-iodoantypyrine autoradiographic technique. Whereas hypotension alone (40-50 mmHg) resulted in neither ischaemic brain damage nor significant alterations in cerebral blood flow, the combination of this degree of hypotension with unilateral carotid occlusion produced predominantly unilateral ischaemic brain damage which correlated with regions of reduced cerebral blood flow. With this type of haemodynamically induced oligaemia, the most vulnerable areas were the lateral neocortex, the caudate nucleus, the hippocampus and the thalamus. Within the cortex, the greatest reductions in blood flow occurred in the deeper cortical layers, and this was the most frequent site of ischaemic cell change. These data support the concept of a haemodynamic mechanism in the pathogenesis of some transient cerebral ischaemic attacks in man.