Embolic stroke in aged rats.

BACKGROUND AND PURPOSE Although stroke is a disorder associated with aging, experimental studies of stroke are conducted in young adult (2-4-month-old) animals (rat life span, 27-29 months). To determine whether histopathologic changes caused by cerebral infarction would be altered in aged animals, we produced embolic cerebral infarction in 17 aged (23-24-month-old) and 16 young (2-4-month-old) rats. METHODS The right common carotid artery was irradiated with a laser (632 nm, 200 mW/cm2, 15-20 minutes) after the intravenous injection of the photosensitizing dye Photofrin II (12.5 mg/kg). This produces a nonocclusive platelet thrombus that spontaneously embolizes to the brain. Animals were killed 4 days later. RESULTS Analysis was done on 142 infarcts, 68 in aged rats and 74 in young rats. Hypercellularity, with infiltration of macrophages, was more common within small infarcts (less than 1 mm) in young than in aged rats (p = 0.002), and hypertrophy of astroglial fibers surrounding the infarcts was more prominent in young rats. Larger infarcts (greater than or equal to 1 mm) were often hypocellular, with a trend toward more macrophages in the periphery of the infarcts in young than in old animals (p = 0.170). CONCLUSIONS The infiltration of macrophages into cerebral infarcts and the hypertrophy of astroglial fibrils surrounding these infarcts are reduced in the aged rat. These age-related differences emphasize the importance of using appropriately aged animals in experimental models of stroke.