title: Cerebral blood flow at one year after controlled cortical impact in rats: assessment by magnetic resonance imaging.
abstract: Progressive tissue loss and delayed cognitive deficits are seen in rats during the initial year after experimental traumatic brain injury (TBI). As much as 10% of parenchymal volume is lost even in the contralateral hemisphere by 1 year after controlled cortical impact (CCI) in rats. Progressive declines in cerebral blood flow (CBF) are also associated with advanced age and neurodegenerative diseases. Surprisingly, the long-term effects of TBI on CBF remain undefined. CBF was quantified by continuous arterial spin-labeled magnetic resonance imaging (MRI) and measurements of spin-lattice relaxation time in a slice through the plane of injury at 1 year after experimental TBI produced by CCI (n = 4) or sham surgery (n = 4) in rats. CBF was quantified in six regions of interest (ROIs) that were anatomically identified on the control images in each hemisphere and included a medial cortical segment (contusion-enriched, beneath the impact site, on the ipsilateral side) cortex, hippocampus, thalamus, amygdala/pyriform cortex, and hemisphere. At 1 year after injury, CBF was dramatically (96%) reduced in structures within the large cystic lesion that was seen in three of four rats and variably included cortex and hippocampus. Overall, there was an 80% reduction in CBF in the ipsilateral medial cortical segment comparing CCI and sham groups. Similarly, 52% and 67% reductions were seen in CBF in the cortical and hippocampal ROIs ipsilateral to impact (CCI vs. sham), respectively. These are regions both with marked CBF disturbances early after injury and that ultimately suffer considerable tissue loss over the 1-year interval. However, at 1 year after CCI, CBF was not different from sham in other ROIs, including ipsilateral thalamus, or either contralateral hippocampus or hemisphere. We conclude that, at 1 year after CCI, CBF is reduced in anatomic structures at or near the impact site, including injured cortex and hippocampus, and this translates into a reduction in hemispheric CBF. However, despite both significant occult tissue loss ipsilateral and contralateral to the injury and delayed cognitive deficits, widespread reductions in CBF are not observed. This suggests the possibility of remodeling or repackaging of the brain that preserves CBF outside of the cystic lesion.
authors.affiliation: Department of Critical Care Medicine and Anesthesiology, Center for Resuscitation Research, Pittsburgh, Pennsylvania 15260, USA. Kochanekpm@ccm.upmc.edu
authors.forename: Patrick M
authors.initials: PM
authors.lastname: Kochanek
authors.forename: Kristy S
authors.initials: KS
authors.lastname: Hendrich
authors.forename: C Edward
authors.initials: CE
authors.lastname: Dixon
authors.forename: Joanne K
authors.initials: JK
authors.lastname: Schiding
authors.forename: Donald S
authors.initials: DS
authors.lastname: Williams
authors.forename: Chien
authors.initials: C
authors.lastname: Ho
mesh_terms: D000818:Animals; D001921:Brain / Q000098:blood supply*; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D008279:Magnetic Resonance Imaging; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013113:Spin Labels; D013997:Time Factors
chemical_list: D013113:Spin Labels