ASSESSMENT OF CEREBRAL BLOOD-FLOW AND CO2 REACTIVITY AFTER CONTROLLEDCORTICAL IMPACT BY PERFUSION MAGNETIC-RESONANCE-IMAGING USING ARTERIAL SPIN-LABELING IN RATS

We measured CBF and CO, reactivity after traumatic brain injury (TBI) produced by controlled cortical impact (CCI) using magnetic resonance imaging (MRI) and spin-labeled carotid artery water protons as an endo genous tracer. Fourteen Sprague-Dawley rats divided into TBI (CCI; 4.0 2 +/- 0.14 m/s velocity; 2.5 mm deformation), sham, and control groups were studied 24 hours after TBI or surgery. Perfusion maps were gener ated during normocarbia (PaCO2 30 to 40 mm Hg) and hypocarbia (PaCO2 1 5 to 25 mm Hg). During normocarbia, CBF was reduced within a cortical region of interest (ROI, injured versus contralateral) after TBI (200 +/- 82 versus 296 +/- 65 mL.100 g(-1).min(-1), P < 0.05). Within a con tusion-enriched ROI, CBF was reduced after TBI (142 +/- 73 versus 280 +/- 64 mL.100 g(-1).min(-1), P < 0.05). Cerebral blood flow in the sha m group was modestly reduced (212 +/- 112 versus 262 +/- 118 mL.100 g( -1).min(-1), P < 0.05). Also, TBI widened the distribution of CBF in i njured and contralateral cortex. Hypocarbia reduced cortical CBF in co ntrol (48%), sham (45%), and TBI rats (48%) versus normocarbia, P < 0. 05. In the contusion-enriched ROI, only controls showed a significant reduction in CBF, suggesting blunted CO2 reactivity in the sham and TB I group. CO2 reactivity was reduced in the sham (13%) and TBI (30%) gr oups within the cortical ROI (versus contralateral cortex). These valu es were increased twofold within the contusion-enriched ROI but were n ot statistically significant. After TBI, hypocarbia narrowed the CBF d istribution in the injured cortex. We conclude that perfusion MRI usin g arterial spin-labeling is feasible for the serial, noninvasive measu rement of CBF and CO2 reactivity in rats.