caa a22 4500 357894367 CHVBK 20170617161442.0 cr unu---uuuuu 160308s2016 xx s 000 0 eng 10.1007/s11910-016-0638-5 doi (SERVAL)BIB_881133C464C1 26898683 pmid 000371174700003 isiid Cerebral Lactate Metabolism After Traumatic Brain Injury [Elektronische Daten] [C. Patet, T. Suys, L. Carteron, M. Oddo] Cerebral energy dysfunction has emerged as an important determinant of prognosis following traumatic brain injury (TBI). A number of studies using cerebral microdialysis, positron emission tomography, and jugular bulb oximetry to explore cerebral metabolism in patients with TBI have demonstrated a critical decrease in the availability of the main energy substrate of brain cells (i.e., glucose). Energy dysfunction induces adaptations of cerebral metabolism that include the utilization of alternative energy resources that the brain constitutively has, such as lactate. Two decades of experimental and human investigations have convincingly shown that lactate stands as a major actor of cerebral metabolism. Glutamate-induced activation of glycolysis stimulates lactate production from glucose in astrocytes, with subsequent lactate transfer to neurons (astrocyte-neuron lactate shuttle). Lactate is not only used as an extra energy substrate but also acts as a signaling molecule and regulator of systemic and brain glucose use in the cerebral circulation. In animal models of brain injury (e.g., TBI, stroke), supplementation with exogenous lactate exerts significant neuroprotection. Here, we summarize the main clinical studies showing the pivotal role of lactate and cerebral lactate metabolism after TBI. We also review pilot interventional studies that examined exogenous lactate supplementation in patients with TBI and found hypertonic lactate infusions had several beneficial properties on the injured brain, including decrease of brain edema, improvement of neuroenergetics via a "cerebral glucose-sparing effect," and increase of cerebral blood flow. Hypertonic lactate represents a promising area of therapeutic investigation; however, larger studies are needed to further examine mechanisms of action and impact on outcome. Patet C. aut Suys T. aut Carteron L. aut Oddo M. aut Current Neurology and Neuroscience Reports 16/4(2016), 31 16:4<31 2016 16 1 article serval SERVAL 700 1- Patet C. aut SERVAL 700 1- Suys T. aut SERVAL 700 1- Carteron L. aut SERVAL 700 1- Oddo M. aut SERVAL 773 0- Current Neurology and Neuroscience Reports 16/4(2016), 31 16:4<31 2016 16 BK010053 XK010053 XK010000 SERVAL SERVAL SERVAL article