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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.
Futrell et al. (Sun,) studied this question.