E-111 Analysis of intracerebral hemorrhage in n established mouse model

BackgroundKontos’ elucidated the theory that iron-mediated free radical production and subsequent oxidative damage was responsible for on-going cerebral degeneration within the infarct following ischemic stroke. The production of free radicals is likely tied to the generation of superoxide following reperfusion of the ischemic brain. Free radical production happens relatively soon after reperfusion but the time to oxidative damage of surrounding tissue is still unknown. It is well-established that ischemic stroke results in loss of autoregulation to cerebral tissues. Ischemic strokes have the potential to transform into hemorrhagic lesions. There is less known about the timeline of oxidative damage to the surrounding tissues after the point of transformative hemorrhage. We characterized the initial intracerebral hemorrhage (ICH) event with an in-house mouse model and tracked oxidative biomarkers in the hemorrhagic core, peri-hematoma zone, contralateral brain tissue and in sham mice using Fourier transform infrared (FTIR) imaging and X-ray fluorescence imaging (XFI) at consecutive time points post-ICH. We strive to provide a clear picture of the natural history of events that occur following the hemorrhagic transformation of ischemic stroke. We also strive to identify intervenable chemical processes and biomolecular targets for subsequent treatments aimed at preventing collateral damage to healthy brain tissue.MethodsMice are anesthetized using isoflurane, followed by p...
Source: Journal of NeuroInterventional Surgery - Category: Neurosurgery Authors: Tags: SNIS 19th annual meeting electronic poster abstracts Source Type: research