Brain tissue hypoxia is a common consequence of traumatic brain injury (TBI) due to the rupture of blood vessels during impact and it correlates with poor outcome. The current magnetic resonance imaging (MRI) techniques are unable to provide a direct map of tissue hypoxia.
To investigate whether GdDO3NI, a nitroimidazole‐based T1MRI contrast agent allows imaging hypoxia in the injured brain after experimental TBI.
Prospective.
TBI‐induced mice (controlled cortical impact model) were intravenously injected with either conventional T1agent (gadoteridol) or GdDO3NI at 0.3 mmol/kg dose (
7 T/T2‐weighted spin echo and T1‐weighted gradient echo.
Injured animals were imaged with T2‐weighted spin‐echo sequence to estimate the extent of the injury. The mice were then imaged precontrast and postcontrast using a T1‐weighted gradient‐echo sequence for 3 hours postcontrast. Regions of interests were drawn on the brain injury region, the contralateral brain as well as on the cheek muscle region for comparison of contrast kinetics. Brains were harvested immediately post‐imaging for immunohistochemical analysis.
One‐way analysis of variance and two‐sample
GdDO3NI retention in the injury region at 2.5–3 hours post‐injection was significantly higher compared to gadoteridol (mean retention fraction 63.95% ± 27.43% vs. 20.68% ± 7.43% for gadoteridol at 3 hours) while it rapidly cleared out of the muscle region. Pimonidazole staining confirmed the presence of hypoxia in both gadoteridol and GdDO3NI cohorts, and the later cohort showed good agreement with MRI contrast enhancement.
GdDO3NI was successfully shown to visualize hypoxia in the brain post‐TBI using T1‐weighted MRI at 2.5–3 hours postcontrast.
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