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Clinical studies suggest that increased cerebral blood flow (CBF), or hyperemia, after traumatic brain injury (TBI) is commonly found in children and young adults, but is less often found in adults older than 40 years. However, whether posttraumatic cerebral hyperemia is truly an age-related phenomenon has not been proven. Using a model of focal percussive TBI, we hypothesized that (1) local CBF (ICBF) is increased by 24 after injury, and (2) the magnitude of the ICBF increase is age-related and is greatest in immature rats. Wistar rats that were immature (3.5-4.5 weeks), mature (2-3 months), and aged (14.5-15.5 months) were anesthetized and ventilated. TBI was produced by dropping a weight on the exposed right parietal cortex. LCBF was determined by [(14)C]iodoan-tipyrine autoradiography at 24 h posttrauma in all three age groups, at 48 h posttrauma in immature and mature rats, and at 7 days posttrauma in mature rats. In all age groups, low ICBF (<50 mL 100 g(-1) min(-1)) was present in the area of impact at all times studied. At 24 h, hyperemia was observed (vs. corresponding regions of age-matched control rats) in immature and mature rats (7/17 and 5/17 regions, respectively, both p < 0.05), but not in aged rats. Comparisons of ICBF between the three age groups revealed a hyperemic response in the peritrauma region in immature rats. Hyperemia persisted to 48 h in both immature and mature rats (2 and 7 of 17 structures with increased ICBF in immature and mature rats, respectively, both p < .05). By 7 days posttrauma no regions of increased ICBF were found. Posttraumatic hyperemia appears to be an age-dependent phenomenon. These results suggest possible age-related differences in vasoreactivity or regional metabolism after TBI.

Clinical studies suggest that children respond to head injury with more pronounced cerebral edema and hyperemia than do adults. We hypothesized that these age-related differences could be demonstrated in an animal model. Anesthetized and ventilated mature (2-3 months) and immature (3.5-4.5 weeks) male Wistar rats were traumatized by weight drop onto the exposed right parietal cortex. Trauma severity was adjusted to keep the ratio of force to brain weight constant. This resulted in an energy delivered to the brain of about 9 x 10(3) ergs.mm-2.g-1 brain in both age groups. Percent right hemispheric brain water (%RBW) was measured at 2, 24, 48, and 168 h posttrauma. Infarct area, intracranial pressure (ICP), and 14C-iodoantipyrine autoradiographic local cerebral blood flow (ICBF) were measured at 2 h or 24 h posttrauma. In mature rats, %RBW was unchanged at 2 h, but increased at 24 and 48 h (both p < 0.05). In immature rats, %RBW increased at 2 h and remained elevated at 24 and 48 h (all p < 0.05). Traumatic infarct area as a percent of hemispheric area at 24 h did not differ between age groups. In mature rats, at 2 h posttrauma ICBF was reduced (p < 0.05) in 16 of 17 regions but in only 4 of 17 regions in immature rats. ICBF as a percent of age-matched control values showed a greater reduction in mature vs immature rats in 9 of 16 regions (p < 0.05). ICP increased at 24 h posttrauma in both age groups. In immature rats posttrauma, brain water increased earlier and cerebral hypoperfusion was less marked than in mature rats.