A cold-lesion injury of mild degree was induced in the parietal cortex of adult rats by application of a cooled metal plate. Twenty four hours after injury, the ultrastructure of the micro-blood vessels in the edema area was observed, following intravenous administration of horseradish peroxidase (HRP). The circulation time of HRP was restricted to a maximum of 40 min and the transit time of HRP across the cerebral endothelium of the edema area was investigated morphologically. At least 5 min was required for intravenously injected HRP to cross the endothelium in the area of vasogenic brain edema following cold-lesion injury. In addition to the capillaries, the arterioles appeared to play an important role in the increased permeability of cerebral blood vessels after cold-lesion injury. The increased permeability was thought to be due to increased vesicular transport and damage to endothelial plasma membranes, but the priority of these factors could not be determined using this method.