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Due to the rapid and complex progression of metabolic alteration after traumatic brain injury (TBI), prompt assessment of cerebral metabolism is critical in preventing the subsequent injury processes and developing proper therapeutic strategies. In this study, we assessed longitudinal changes in bicarbonate production from hyperpolarized 1-13Cpyruvate in a rat TBI model. In addition to elevated lactate production, we observed significantly reduced bicarbonate production in the injured site. The contrast of bicarbonate signals between the injured region and the contralateral brain peaked at one day post-injury. A subset of TBI rats demonstrated markedly increased bicarbonate in contralateral brain regions post-injury.
Chen et al. (Wed,) studied this question.