• Transl Stroke Res · Aug 2015

    Correlating Cerebral (18)FDG PET-CT Patterns with Histological Analysis During Early Brain Injury in a Rat Subarachnoid Hemorrhage Model.

    • Jianping Song, Peiliang Li, Neeraj Chaudhary, Joseph J Gemmete, B Gregory Thompson, Guohua Xi, and Aditya S Pandey.
    • Department of Neurosurgery, University of Michigan, 1500 E. Medical Center Dr., Room 3552 TC, Ann Arbor, MI, 48109-5338, USA.
    • Transl Stroke Res. 2015 Aug 1; 6 (4): 290-5.

    AbstractEarly brain injury (EBI) plays a significant role in poor outcomes for subarachnoid hemorrhage (SAH) patients. Further investigations are required to characterize the cellular metabolic and related histological changes that may contribute to EBI following SAH. We investigated the image patterns of 18-fluorodeoxyglucose positron emission tomography-computed tomography ((18)FDG PET-CT) during EBI and correlated histopathological changes utilizing a rat SAH model. SAH was induced in six adult male Sprague-Dawley rats by endovascular perforation, and animals were randomly assigned to receive (18)FDG PET-CT imaging at either 3 or 12 h post-procedure. Mean (18)FDG standard uptake value (SUV) of the brain was calculated. Animals were euthanized 48 h post-procedure, and brain samples were used for heme oxygenase-1 (HO-1) and dopamine- and cAMP-regulated phosphoprotein (DARPP-32) Mr 32 kDa immunohistochemistry. Rats within the SAH group had higher mean whole brain (18)FDG SUV (2.349 ± 0.376 g/ml in the 3-h group and 2.453 ± 0.495 g/ml in the 12-h group) compared to that of sham (n = 3; mean SUV = 2.030 ± 0.247 g/ml; P < 0.05) or control groups (n = 3; mean SUV = 1.800 ± 0.484 g/ml; P < 0.05). Whole brain (18)FDG SUV did not vary significantly between rats imaged at 3 h vs. those imaged at 12 h post-SAH (P > 0.05). Regions of decreasing SUV in SAH rats correlated with neuronal death and increased expression of HO-1. Higher (18)FDG PET SUV was evident in rats post-SAH compared to sham and control groups. Regions of decreasing SUV in SAH rats correlated with neuronal death and increased HO-1 expression as evaluated by histopathology.

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